We all want to be happy.

And there is no shortage of advice on what we need to do to lead happy, fulfilled lives. There are even “experts” who offer advice on what we shouldn’t do, if we want to be happy.

As a scientist, there is one thing that makes me (and most other scientists) giddy with delight: It is learning how things in nature work.

Most scientists have a burning curiosity to understand the world around them, me included. Like most scientists, I derive enormous amount of joy and satisfaction when I gain insight into the inner workings of some feature of nature. And, like most in the scientific community, I feel frustrated and disappointed when I don’t know why things are the way they are. Side by side, this combination of joy and frustration serves as one of the driving forces for my work as a scientist.

And, because many of the most interesting questions in science can appear at times to be nearly impenetrable mysteries, new discoveries typically bring me (and most other scientists) a mixture of hope and consternation.

Trying to Solve a Mystery

These mixed emotions are clearly evident in the life scientists who strive to understand the evolutionary origin of complex, eukaryotic cells. As science journalist Carl Zimmer rightly points out, the evolutionary process that produced eukaryotic cells from simpler microbes stands as “one of the deepest mysteries in biology.”¹ And while researchers continue to accumulate clues about the origin of eukaryotic cells, they remain stymied when it comes to offering a robust, reliable evolutionary account of one of life’s key transitions.

The leading explanation for the evolutionary origin of eukaryotic cells is the endosymbiont hypothesis. On the surface, this idea appears to be well evidenced. But digging a little deeper into the details of this model exposes gaping holes. And each time researchers present new understanding about this presumed evolutionary transition, it exposes even more flaws with the model, turning the joy of discovery into frustration, as the latest work by a team of Japanese microbiologists attests.²

Before we unpack the work by the Japanese investigators and its implications for the endosymbiont hypothesis, a quick review of this cornerstone idea in evolutionary theory is in order. (If you are familiar with the endosymbiont hypothesis and the evidence in support of the model, please feel free to skip ahead to The Discovery of Lokiarchaeota)

The Endosymbiont Hypothesis

According to this idea, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe.

Much of the endosymbiont hypothesis centers around the origin of the mitochondrion. Presumably, this organelle started as an endosymbiont. Evolutionary biologists believe that once engulfed by the host cell, this microbe took up permanent residency, growing and dividing inside the host. Over time, the endosymbiont and the host became mutually interdependent, with the endosymbiont providing a metabolic benefit for the host cell, such as supplying a source of ATP. In turn, the host cell provided nutrients to the endosymbiont. Presumably, the endosymbiont gradually evolved into an organelle through a process referred to as genome reduction. This reduction resulted when genes from the endosymbiont’s genome were transferred into the genome of the host organism.

Figure 1: A Depiction of the Endosymbiont Hypothesis. Image credit: Shutterstock

Evidence for the Endosymbiont Hypothesis

At least three lines of evidence bolster the hypothesis:

• The similarity of mitochondria to bacteria. Most of the evidence for the endosymbiont hypothesis centers around the fact that mitochondria are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.
• Mitochondrial DNA. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. They see the biochemical similarities between mitochondrial and bacterial genomes as further evidence for the evolutionary origin of these organelles.
• The presence of the unique lipid, cardiolipin, in the mitochondrial inner membrane. This important lipid component of bacterial inner membranes is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider cardiolipin a signature lipid for mitochondria and another relic from its evolutionary past.

The Discovery of Lokiarchaeota

Evolutionary biologists have also developed other lines of evidence in support of the endosymbiont hypothesis. For example, biochemists have discovered that the genetic core (DNA replication and the transcription and translation of genetic information) of eukaryotic cells resembles that of the Archaea. This similarity suggests to many biologists that a microbe belonging to the archaeal domain served as the host cell that gave rise to eukaryotic cells.

Life scientists think they may have made strides toward identifying the archaeal host. In 2015, a large international team of collaborators reported the discovery of Lokiarchaeota, a new phylum belonging to the Archaea. This phylum groups with eukaryotes on the evolutionary tree. Analysis of the genomes of Lokiarchaeota reveal the presence of genes that encode for the so-called eukaryotic signature proteins (ESPs). These genes are unique to eukaryotic organisms.³

As exciting as the discovery has been for evolutionary biologists, it has also been a source of frustration. Researchers didn’t discover this group of microbes by isolating microbes and culturing them in the lab. Instead, they discovered them by recovering DNA fragments from the environment (a hydrothermal vent system in the Atlantic Ocean called Loki’s Castle, after Loki, the ancient Norse god of trickery) and assembling them into genome sequences. Through this process, they learned that Lokiarchaeota correspond to a new group of Archaea, called the Asgardians. The reconstructed Lokiarchaeota “genome” is low quality (1.4-fold coverage) and incomplete (8 percent of the genome is missing).

Mystery Solved?

So, without actual microbes to study, the best that life scientists could do was infer the cell biology of Lokiarchaeota from its genome. But this frustrating limitation recently turned into excitement as a team of Japanese microbiologists isolated and cultured the first microbe that belongs to this group of archaeons, dubbed Prometheoarchaeum syntrophicum. It took researchers nearly 12 years of laboratory work to isolate this slow-growing microbe from sediments in the Pacific Ocean and culture it in the laboratory. (It takes 14 to 25 days for the microbe to double.) But this effort is now paying off, because the research team is now able to get a glimpse into what many life scientists believe to be a representative of the host microbe that spawned the first eukaryotic cells.

P. syntrophicum is spherically shaped and about 550 nm in size. In culture, this microbe forms aggregates around an extracellular polymeric material it secretes. It also has unusual membrane-based tentacle-like protrusions (of about 80 to 100 nm in length) that extend from the cell surface.

Researchers were unable to produce a pure culture of P. syntrophicum because it forms a close association with other microbes. The team learned that P. syntrophicum lives a syntrophic lifestyle, meaning that it forms interdependent relationships with other microbes in the environment. Specifically, P. syntrophicum produces hydrogen and formate as metabolic by-products that, in turn, are scavenged for nutrients by partner microbes. Researchers also discovered that P. syntrophicum consumes amino acids externally supplied in the growth medium. Presumably, this observation means that in the ocean floor sediments, P. syntrophicum feeds on organic materials released by its microbial counterpart.

P. syntrophicum and Failed Predictions of the Endosymbiont Hypothesis

Availability of P. syntrophicum cells now allows researchers the unprecedented chance to study a microbe that they believe stands in as a representative for the archaeal host in the endosymbiont hypothesis. Has the mystery been solved? Instead of affirming the scientific predictions of leading versions of the endosymbiont hypothesis, the biology of this organism adds to the frustration and confusion surrounding the evolutionary account. Scientific analysis produces raises three questions for the evolutionary view:

• First, this microbe has no internal cellular structures. This observation stands as a failed prediction. Because Lokiarchaeota (and other members of the Asgard archaeons) have a large number of ESPs present in their genomes, some biologists speculated that the Asgardian microbes would have complex subcellular structures. Yet, this expectation has not been realized for P. syntrophicum, even though this microbe has around 80 or so ESPs in its genome.
• Second, this microbe can’t engulf other microbes. This inability also serves as a failed prediction. Prior to the cultivation of P. syntrophicum, analysis of the genomes of Lokiarchaeota identified a number of genes involved in membrane-related activities, suggesting that this microbe may well have possessed the ability to engulf other microbes. Again, this expectation wasn’t realized for P. syntrophicum. This observation is a significant blow to the endosymbiont hypothesis, which requires the host cell to have cellular processes in place to engulf other microbes.
• Third, the membranes of this microbe are comprised of typical archaeal lipids and lack the enzymatic machinery to make typical bacterial lipids. This also serves as a failed prediction. Evolutionary biologists had hoped that P. syntrophicum would provide a solution to the lipid divide (next section). It doesn’t.

What Is the Lipid Divide?

The lipid divide refers to the difference in the chemical composition of the cell membranes found in bacteria and archaea. Phospholipids comprise the cell membranes of both sorts of microbes. But that‘s where the similarity ends. The chemical makeup of the phospholipids is distinct in bacteria and archaea, respectively.

Bacterial phospholipids are built around a D-glycerol backbone which has a phosphate moiety bound to the glycerol in the sn-3 position. Two fatty acids are bound to the D-glycerol backbone at the sn-1 and sn-2 position. In water, these phospholipids assemble into bilayer structures.

Archaeal phospholipids are constructed around an L–glycerol backbone (which produces membrane lipids with different stereochemistry than bacterial phospholipids). The phosphate moiety is attached to the sn-1 position of glycerol. Two isoprene chains are bound to the sn-2 and sn-3 positions of L-glycerol via ether linkages. Some archaeal membranes are formed from phospholipid bilayers, while others are formed from phospholipid monolayers.

Presumably, the structural features of the archaeal phospholipids serve as an adaptation that renders them ideally suited to form stable membranes in the physically and chemically harsh environments in which many archaea find themselves.

The Lipid Divide Frustrates the Endosymbiont Hypothesis

If the host cell in the endosymbiont evolutionary mechanism is an archaeal cell, it logically follows that the membrane composition of eukaryotic cells should be archaeal-like. As it turns out, this expectation is not met. The cell membranes of eukaryotic cells closely resemble bacterial, not archaeal, membranes.

Can Lokiarchaeota Traverse the Lipid Divide?

Researchers had hoped that the discovery of Lokiarchaeota would shed light on the evolutionary origin of eukaryotic cell membranes. In the absence of having actual organisms to study, researchers screened the Lokiarchaeota genome for enzymes that would take part in phospholipid synthesis, with the hopes of finding clues about how this transition may have occurred.

Based on their analysis, they argued that Lokiarchaeota could produce some type of hybrid phospholipid with features of both archaeal and bacterial phospholipids. Still, their conclusion remained speculative at best. The only way to establish Lokiarchaeota membranes as transitional between those found in archaea and bacteria is to perform chemical analysis of its membranes. With the isolation and cultivation of P. syntrophicum this analysis is possible. Yet its results only serve to disappoint evolutionary biologists, because this microbe has typical archaeal lipids in its membranes and displays no evidence of being capable of making archaeal/bacterial hybrid lipids.

A New Model for the Endosymbiont Hypothesis?

Not to be dissuaded by these disappointing results, the Japanese researchers propose a new version of the endosymbiont hypothesis, consistent with P. syntrophicum biology. For this model, they envision the archaeal host entangling an oxygen-metabolizing, ATP-producing bacterium in the tentacle-like structures that emanate from its cellular surface. Over time, the entangled organism forms a mutualistic relationship with the archaeal host. Eventually, the host encapsulates the entangled microbe in an extracellular structure that forms the body of the eukaryotic cell, with the host cell forming a proto-nucleus.

Though this model is consistent with P. syntrophicum biology, it is highly speculative and lack supporting evidence. To be fair, the Japanese researchers make this very point when they state, “further evidence is required to support this conjecture.”⁵

This work shows how scientific advance helps validate or invalidate models. Even though many biologists view the endosymbiont hypothesis as a compelling, well-established theory, significant gaps in our understanding of the origin of eukaryotic cells persist. (For a more extensive discussion of these outages see the Resources section.) In my view as a biochemist, some of these gaps are unbridgeable chasms that motivate my skepticism about the endosymbiont hypothesis, specifically, and the evolutionary approach to explain the origin of eukaryotic cells, generally.

Of course, my skepticism leads to another question: Is it possible that the origin of eukaryotic cells reflects a Creator’s handiwork? I am happy to say that the answer is “yes.”

Resources

Challenges to the Endosymbiont Hypothesis

• “Evolutionary Paradigm Lacks Explanation for Origin of Mitochondria and Eukaryotic Cells” by Fazale Rana (article)
• “Complex Protein Biogenesis Hints at Intelligent Design” by Fazale Rana (article)
• “ATP Transport Challenges the Evolutionary Origin of Mitochondria” by Fazale Rana (article)
• “Membrane Biochemistry Challenges Route to Evolutionary Origin of Complex Cells” by Fazale Rana (article)
• “Endosymbiont Hypothesis: Things Aren’t What They Seem to Be” by Fazale Rana (article)

In Support of A Creation Model for the Origin of Eukaryotic Cells

• “Endosymbiont Hypothesis and the Ironic Case for a Creator” by Fazale Rana (article)
• “Why Do Mitochondria Have DNA?” by Fazale Rana (article)
• “Mitochondrial Genomes: Evidence for Evolution or Creation?” by Fazale Rana (article)
• “Mitochondria’s Deviant Genetic Code: Creation or Evolution?” by Fazale Rana (article)
• “Can a Creation Model Explain the Origin of Mitochondria?” by Fazale Rana (article)
• “Molecular Logic of the Electron Transport Chain Supports Creation” by Fazale Rana (article)
• “Why Mitochondria Make My List of Best Biological Designs” by Fazale Rana (article)

Truth be told, we all hold to certain stereotypes whether we want to admit it or not. Though unfair, more often than not, these stereotypes cause little real damage.

Yet, there are instances when stereotypes can be harmful—even deadly. As a case in point, researchers have shown that stereotyping disrupts the healthcare received by members of so-called disadvantaged groups, such as African Americans, Latinos, and the poor.¹

Healthcare providers are frequently guilty of bias towards underprivileged people. Often, the stereotyping is unconscious and unintentional. Still, this bias compromises the medical care received by people in these ethnic and socioeconomic groups.

Underprivileged patients are also guilty of stereotyping. It is not uncommon for these patients to perceive themselves as the victims of prejudice, even when their healthcare providers are genuinely unbiased. As a result, these patients don’t trust healthcare workers and, consequently, withhold information that is vital for a proper diagnosis.

Fortunately, psychologists have developed best practices that can reduce stereotyping by both healthcare practitioners and patients. Hopefully, by implementing these practices, the impact of stereotyping on the quality of healthcare can be minimized over time.

Recently, a research team from Australia identified another form of stereotyping that holds the potential to negatively impact healthcare outcomes.² In this case, the impact of this stereotyping isn’t limited to disadvantaged people; it affects all of us.

A Bias Against Pseudogenes

These researchers have uncovered a bias in the way life scientists view the human genome (and the genomes of other organisms). Too often they regard the human genome as a repository of useless, nonfunctional DNA that arises as a vestige of evolutionary history. Because of this view, life scientists and the biomedical research community eschew studying regions of the human genome they deem to be junk DNA. This posture is not unreasonable. It doesn’t make sense to invest precious scientific resources to study nonfunctional DNA.

Many life scientists are unaware of their bias. Unfortunately, this stereotyping hinders scientific advance by delaying discoveries that could be translated into the clinical setting. Quite often, supposed junk DNA has turned out to serve a vital purpose. Failure to recognize this function not only compromises our understanding of genome biology, but also hinders biomedical researchers from identifying defects in these genomic regions that contribute to genetic diseases and disorders.

As psychologists will point out, acknowledging bias is the first step to solving the problems that stereotyping causes. This is precisely what these researchers have done by publishing an article in Nature Review Genetics.³ The team focused on DNA sequence elements called pseudogenes. Traditionally, life scientists have viewed pseudogenes as the remnants of once functional genes. Biologists have identified three categories of pseudogenes: (1) unitary, (2) duplicated, and (3) processed.

Researchers categorize DNA sequences as pseudogenes based on structural features. Such features indicate to the investigators that these sequence elements were functional genes at one time in evolutionary history, but eventually lost function due to mutations or other biochemical processes, such as reverse transcription and DNA insertion. Once a DNA sequence is labeled a pseudogene, bias sets in and researchers just assume that it lacks function—not because it has been experimentally demonstrated to be nonfunctional, but because of the stereotyping that arises out of the evolutionary paradigm.

The authors of the piece acknowledge that “the annotation of genomics regions as pseudogenes constitutes an etymological signifier that an element has no function and is not a gene. As a result, pseudogene-annotated regions are largely excluded from functional screen and genomic analyses.”⁴ In other words, the “pseudogene” moniker biases researchers to such a degree that they ignore these sequence elements as they study genome structure and function without ever doing the hard, experimental work to determine whether it is actually nonfunctional.

This approach is clearly misguided and detracts from scientific discovery. As the authors admit, “However, with a growing number of instances of pseudogene-annotated regions later found to exhibit biological function, there is an emerging risk that these regions of the genome are prematurely dismissed as pseudogenic and therefore regarded as void of function.”⁵

Discovering Function Despite Bias

The harmful effects of this bias become evident as biomedical researchers unexpectedly stumble upon function for pseudogenes, time and time, again, not because of the evolutionary paradigm, but despite it. These authors point out that many processed pseudogenes are transcribed and, of those, many are translated to produce proteins. Many unitary and duplicated pseudogenes are also transcribed. Some are also translated into proteins, but a majority are not. Instead they play a role in gene regulation as described by the competitive endogenous RNA hypothesis.

Still, there are some pseudogenes that aren’t transcribed and, thus, could rightly be deemed nonfunctional. However, the researchers point out that the current experimental approaches for identifying transcribed regions are less than ideal. Many of these methods may fail to detect pseudogene transcripts. However, as the researchers point out, even if a pseudogene isn’t transcribed it still may serve a functional role (e.g., contributing to chromosome three-dimensional structure and stability).

This Nature article raises a number of questions and concerns for me as a biochemist:

• How widespread is this bias?
• If this type of stereotyping exists toward pseudogenes, does it exist for other classes of junk DNA?
• How well do we really understand genome structure and function?
• Do we have the wrong perspective on the genome, one that stultifies scientific advance?
• Does this bias delay the understanding and alleviation of human health concerns?

Is the Evolutionary Paradigm the Wrong Framework to Study Genomes?

Based on this article, I think it is safe to conclude that we really don’t understand the molecular biology of genomes. We are living in the midst of a scientific revolution that is radically changing our view of genome structure and function. The architecture and operations of genomes appear to be far more elegant and sophisticated than anyone ever imagined—at least within the confines of the evolutionary paradigm.

This insight also leads me to question if the evolutionary paradigm is the proper framework for thinking about genome structure and function. From my perspective, treating biological systems as the Creator’s handiwork provides a superior approach to understanding the genome. A creation model approach promotes scientific advance, particularly when the rationale for the structure and function of a particular biological system is not apparent. This expectation forces researchers to keep an open mind and drives further study of seemingly nonfunctional, purposeless systems with the full anticipation that their functional roles will eventually be uncovered.

Over the last several years, I have raised concerns about the bias life scientists have harbored as they have worked to characterize the human genome (and genomes of other organisms). It is gratifying to me to see that there are life scientists who, though committed to the evolutionary paradigm, are beginning to recognize this bias as well.

The first step to addressing the problem of stereotyping—in any sector of society—is to acknowledge that it exists. Often, this step is the hardest one to take. The next step is to put in place structures to help overcome its harmful influence. Could it be that part of the solution to this instance of scientific stereotyping is to grant a creation model approach access to the scientific table?

Resources

• Who Was Adam? A Creation Model Approach to the Origin of Humanity, 2nd exp. ed., by Fazale Rana with Hugh Ross (book)
• The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)

Pseudogene Function

• “Pseudogene Decoy Reveals Hidden Evidence for Design” by Fazale Rana (article)
• “Functional Pseudogenes Are Everywhere!” by Fazale Rana (article)
• “High Levels of Pseudogene Expression Help Silence the Case for Common Descent” by Fazale Rana (article)
• “Scientific Upset: More Functions for Pseudogenes” by Fazale Rana (article)
• “Pseudogene Discovery Pains Evolutionary Paradigm” by Fazale Rana (article)
• “Unitary Pseudogenes Have Function! Part 1” by Fazale Rana (article)
• “Unitary Pseudogenes Have Function! Part 2” by Fazale Rana (article)
• “Competitive Endogenous RNA Hypothesis Supports the Case for Creation” by Fazale Rana (article)

The Evolutionary Paradigm Hinders Scientific Advance

• “Does the Evolutionary Paradigm Stymie Scientific Advance?” by Fazale Rana (article)
• “Evolution’s Flawed Approach to Science” by Fazale Rana (article)

In high school I was a bit of a troublemaker. It wasn’t out of the ordinary for me to be summoned to Mr. Reynolds’ office—the school’s vice principal—for some misdeed or other. After a few office visits, I quickly learned the value of a good story. If convincing enough, I could defray the accusations leveled against me. All I had to do was create plausible deniability.

Story Telling in the Evolutionary Paradigm

Storytelling isn’t just the purview of a mischievous kid facing the music in the principal’s office, it is part of the construct of science.

Recent work by a team of scientific investigators from the University of Florida (UF) highlights the central role that storytelling plays in evolutionary biology.¹ In fact, it is not uncommon for evolutionary biologists to weave grand narratives that offer plausible evolutionary stories for the emergence of biological or behavioral traits. And, though these accounts seem scientific, they are often unverifiable scientific explanations.

Inspired by Rudyard Kipling’s (1865–1936) book of children’s origin stories, the late evolutionary biologist Stephen Jay Gould (1941–2002) referred to these evolutionary tales as just-so stories. To be fair, others have been critical of Gould’s cynical view of evolutionary accounts, arguing that, in reality, just-so stories in evolutionary biology are actually hypotheses about evolutionary transformations. But still, more often than not, these “hypotheses” appear to be little more than convenient fictions.

An Evolutionary Just-So Story of Moths and Bats

The traditional evolutionary account of ultrasonic sound detection in nocturnal moths serves as a case in point. Moths (and butterflies) belong to one of the most important groups of insects: lepidoptera. This group consists of about 160,000 species, with nocturnal moths comprising over 75 percent of the group.

Moths play a key role in ecosystems. For example, they serve as one of the primary food sources for bats. Bats use echolocation to help them locate moths at night. Bats emit ultrasonic cries that bounce off the moths and reflect back to the bats, giving these predators the pinpoint location of the moths, even during flight.

Many nocturnal moth species have defenses that help them escape predation by bats. One defense is ears (located in different areas of their bodies) that detect ultrasonic sounds. This capability allows the moths to hear the bats coming and get out of their way.

For nearly a half century, evolutionary biologists explained moths’ ability to hear ultrasonic sounds as the outworking of an “evolutionary arms race” between echolocating bats and nocturnal moths. Presumably, bats evolved the ability to echolocate, allowing them to detect and prey upon moths at night by plucking them out of the air in mid-flight. In response, some groups of moths evolved ears that allowed them to detect the ultrasonic screeches emitted by bats, helping them to avoid detection.

Figure: Flying Pipistrelle bat. Image credit: Shutterstock

For 50 years, biologists have studied the relationship between echolocating bats and nocturnal moths with the assumption that this explanation is true. (I doubt Mr. Reynolds ever assumed my stories were true.) In fact, evolutionary accounts like this one provide evidence for the idea of coevolution. Advanced by Paul Ehrlich and Peter Raven in 1964, this evolutionary model maintains that ecosystems are shaped by species that affect one another’s evolution.

If the UF team’s work is to be believed, then it turns out that the story recounting the evolutionary arms race between nocturnal moths and echolocating bats is fictional. As team member Jesse Barber, a researcher who has studied bats and moths, complains, “Most of the introductions I’ve written in my papers [describing the coevolution of bats and moths] are wrong.”²

An Evolutionary Study on the Origin of Moths and Butterflies

To reach this conclusion, the UF team generated the most robust evolutionary tree (phylogeny) for lepidopterans to date. They also developed an understanding of the timing of events in lepidopteran natural history. They were motivated to take on this challenge because of the ecological importance of moths and butterflies. As noted, these insects play a central role in terrestrial ecosystems all over the world and coevolutionary models provide the chief explanations for their place in these ecosystems. But, as the UF researchers note, “These hypotheses have not been rigorously tested, because a robust lepidopteran phylogeny and timing of evolutionary novelties are lacking.”³

To remedy this problem, the researchers built a lepidopteran evolutionary tree from a data set of DNA sequences that collectively specified 2,100 protein-coding genes from 186 lepidopteran species. These species represented all the major divisions within this biological group. Then, they dated the evolutionary timing of key events in lepidopteran natural history from the fossil record.

Based on their analysis, the research team concluded that the first lepidopteran appeared around 300 million years ago. This creature fed on nonvascular plants. Around 240 million years ago, lepidopterans with tubelike proboscises (long, sucking mouthpiece) appeared, allowing these insects to extract nectar from flowering plants.

These results cohere with the coevolutionary model that the first lepidopterans fed internally on plants and, later, externally, as they evolved the ability to access nectar from plants. Flowering plants appear around 260 million years ago, which is about the time that the tubelike proboscis appears in lepidopterans.

But perhaps the most important and stunning finding from their study stems from the appearance of hearing organs in moths. It looks as if these organs arose independently 9 separate times—around 80 to 90 million years ago—well before bats began to echolocate. (The earliest known bat from the fossil record with the capacity to echolocate is around 45 to 50 million years old.)

The UF investigators uncovered another surprising result related to the appearance of butterflies. They discovered that butterflies became diurnal (active in the daytime) around 98 million years ago. According to the traditional evolutionary story, butterflies (which are diurnal) evolved from nocturnal moths when they transitioned to daytime activities to escape predation of echolocating bats, which feed at night. But as with the origin of hearing organs in moths, the transition from nocturnal to diurnal behavior occurred well before the first appearance of echolocating bats and seems to have occurred independently at least two separate times.

It Just Isn’t So

The UF evolutionary biologists’ study demonstrates that the coevolutionary models for the origin of hearing organs in moths and diurnal behavior of butterflies—dominant for over a half century in evolutionary thought—are nothing more than just-so stories. They appear to make sense on the surface but are no closer to the truth than the tales I would weave in Mr. Reynolds’ office.

In light of this discovery, the research team posits two new evolutionary models for the origin of these two traits, respectively. Now scientists think that the evolutionary emergence of hearing organs in moths may have provided these insects the capacity for auditory surveillance of their environment. Their capacity to hear may have helped them detect the low-frequency sounds of flapping bird wings, for example, and avoid predation. Presumably, these same hearing organs later evolved to detect the high-frequency cries of bats. As for the evolutionary origin of diurnal behavior characteristic of butterflies, researchers now speculate that butterflies became diurnal to take advantage of flowers that bloom in the daytime.

Again, on the surface, these explanations seem plausible. But one has to wonder if these models, like their predecessors, are little more than just-so stories. In fact, this study raises a general concern: How much confidence can we place in any evolutionary account? Could it be that other evolutionary accounts are, in reality, good stories, but in the end will turn out to be just as fanciful as the stories written by Rudyard Kipling?

In and of itself, recognizing that many evolutionary models could just be stories doesn’t provide sufficient warrant for skepticism about the evolutionary paradigm. But it does give pause for thought. Plus, two insights from this study raise real concerns about the capacity of evolutionary processes to account for life’s history and diversity:

1. The discovery that ultrasonic hearing in moths arose independently nine separate times
2. The discovery that diurnal behavior in butterflies appeared independently in at least two separate instances

Convergence

Evolutionary biologists use the term convergence to refer to the independent origin of identical or nearly identical biological and behavioral traits in organisms that cluster into unrelated groups.

Convergence isn’t a rare phenomenon or limited to the independent origin of hearing organs in moths and diurnal behavior in butterflies. Instead, it is a widespread occurrence in biology, as evolutionary biologists Simon Conway Morris and George McGhee document in their respective books Life’s Solution and Convergent Evolution. It appears as if the evolutionary process routinely arrives at the same outcome, time and time again.⁴ In fact, biologists observe these repeated outcomes at the ecological, organismal, biochemical, and genetic levels.

From my perspective, the widespread occurrence of convergent evolution is a feature of biology that evolutionary theory can’t explain. I see the widespread occurrence of convergence as a failed scientific prediction of the evolutionary paradigm.

Convergence Should Be Rare, Not Widespread

In effect, chance governs biological and biochemical evolution at its most fundamental level. Evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection, which, too, consists of chance components. The consequences are profound. If evolutionary events could be repeated, the outcome would be dramatically different every time. The inability of evolutionary processes to retrace the same path makes it highly unlikely that the same biological and biochemical designs should appear repeatedly throughout nature.⁵

In support of this view, consider a 2002 landmark study carried out by two Canadian investigators who simulated macroevolutionary processes using autonomously replicating computer programs. In their study, the computer programs operated like digital organisms.⁶ The programs could be placed into different “ecosystems” and, because they replicate autonomously, they could evolve. By monitoring the long-term evolution of these digital organisms, the two researchers determined that evolutionary outcomes are historically contingent and unpredictable. Every time they placed the same digital organism in the same environment, it evolved along a unique trajectory.

In other words, given the historically contingent nature of the evolutionary mechanisms, we would expect convergence to be rare in the biological realm. Yet, biologists continue to uncover example after example of convergent features—some of which are quite astounding.

Bat Echolocation and Convergence

Biologists have discovered one such example of convergence in the origin of echolocating bats. Echolocation appears to have arisen two times independently: once in microbats and once in Rhinolophidae, a superfamily of megabats.⁷ Prior to this discovery, reported in 2000, biologists classified Rhinolophidae as a microbat based on their capability to echolocate. But DNA evidence indicates that this superfamily has greater affinity to megabats than to microbats. This result means that echolocation must have originated separately in the microbats and Rhinolophidae. Researchers have also shown that the same genetic and biochemical changes occurred in microbats and megabats to create their echolocating ability. These changes appear to have taken place in the gene prestin and in its protein-product, prestin.⁸

In other words, we observe two outcomes: (1) the traditional evolutionary accounts for coevolution among echolocating bats, nocturnal moths, and diurnal butterflies turned out to be just-so stories, and (2) the convergence observed in these three groups stands as independent and separate instances of failed predictions of the evolutionary paradigm.

Convergence and the Case for Creation

If the widespread occurrence of convergence can’t be explained through evolutionary theory, then how can it be explained?

It is not unusual for architects and engineers to redeploy the same design features, sometimes in objects, devices, or systems that are completely unrelated to one another. So, instead of viewing convergent features as having emerged through repeated evolutionary outcomes, we could understand them as reflecting the work of a divine mind. From this perspective, the repeated origins of biological features equate to the repeated creations by an intelligent Agent who employs a common set of solutions to address a common set of problems facing unrelated organisms.

Now that’s a story even Mr. Reynolds might believe.

Resources

• The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)

Convergence of Echolocation

• “Echoes of Design: Independent Origins of Echolocation in Bats and Dolphins Challenge Biological Evolution” by Fazale Rana (article)
• “Convergence Drives Evolution Batty” by Fazale Rana (article)
• “Analysis of Genomes Converges on the Case for a Creator” by Fazale Rana (article)
• “Convergence: Evidence for a Single Creator” by Fazale Rana (article)

The Historical Contingency of the Evolutionary Process

• “Inability to Repeat Past Dooms Evolution” by Fazale Rana (article)
• “Historical Contingency and the Improbability of Protein Evolution, Part 1” by Fazale Rana (article)
• “Historical Contingency and the Improbability of Protein Evolution, Part 2” by Fazale Rana (article)
• “Long-Term Evolution Experiment: Evidence for the Evolutionary Paradigm? Part 1” by Fazale Rana (article)
• “Long-Term Evolution Experiment: Evidence for the Evolutionary Paradigm? Part 2” by Fazale Rana (article)

In high school, I spent most Sunday mornings with my family gathered around the TV watching weekly reruns of the old Abbott and Costello movies.

Image: Bud Abbott and Lou Costello. Image credit: Wikipedia

One of my favorite routines has the two comedians trying to help a woman get her parallel-parked car out of a tight parking spot. As Costello takes his place behind the wheel, Abbott tells him to “Go ahead and back up.” And of course, confusion and hilarity follow as Costello repeatedly tries to clarify if he is to “go ahead” or “back up,” finally yelling, “Will you please make up your mind!”

As it turns out, biologists who are trying to account for the origin of mitochondria (through an evolutionary route) are just as confused about directions as Costello. Specifically, they are trying to determine which direction ATP transport occurred in the evolutionary precursors to mitochondria (referred to as pre-mitochondria).

In an attempt to address this question, a research team from the University of Virginia (UVA) has added to the frustration, raising new challenges for evolutionary explanations for the origin of mitochondria. Their work threatens to drive the scientific community off the evolutionary route into the ditch when it comes to explaining the origin of eukaryotic cells.¹

To fully appreciate the problems this work creates for the endosymbiont hypothesis, a little background is in order. (For those familiar with the evidence for the endosymbiont hypothesis, you may want to skip ahead to The Role of Mitochondria.)

The Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis serves as the best explanation for the origin of complex cells.

According to this idea, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe.

The “poster children” of the endosymbiont hypothesis are mitochondria. Presumably, the mitochondria started its evolutionary journey as an endosymbiont. Evolutionary biologists believe that once engulfed by the host cell, this microbe took up permanent residency, growing and dividing inside the host. Over time, the endosymbiont and the host became mutually interdependent, with the endosymbiont providing a metabolic benefit for the host cell (such as providing a source of ATP). In turn, the host cell provided nutrients to the endosymbiont. Presumably, the endosymbiont gradually evolved into an organelle through a process referred to as genome reduction. This reduction resulted when genes from the endosymbiont’s genome were transferred into the genome of the host organism, generating the mitonuclear genome.

Image: Endosymbiont Hypothesis. Image credit: Wikipedia

Evidence for the Endosymbiont Hypothesis

Much of the evidence for the endosymbiotic origin of mitochondria centers around the similarity between mitochondria and bacteria. These organelles are about the same size and shape as typical bacteria and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

Biochemical evidence also exists for the endosymbiont hypothesis. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. They see the biochemical similarities between mitochondrial and bacterial genomes as further evidence for the evolutionary origin of these organelles.

The presence of the unique lipid, cardiolipin, in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. This important lipid component of bacterial inner membranes is absent in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider cardiolipin a signature lipid for mitochondria and a vestige of the organelle’s evolutionary history.

The Role of Mitochondria

Mitochondria serve cells in a number of ways, including:

• Calcium storage
• Calcium signaling
• Signaling with reactive oxygen species
• Regulation of cellular metabolism
• Heat production
• Apoptosis

Arguably one of the most important functions of mitochondria relates to their role in energy conversion. This organelle generates ATP molecules by processing the breakdown products of glycolysis through the tricarboxylic acid cycle and the electron transport chain.

Biochemists refer to ATP as a high-energy compound—it serves as an energy currency for the cell, and most cellular processes are powered by ATP. One way that ATP provides energy is through its conversion to ADP and an inorganic phosphate molecule. This breakdown reaction liberates energy that can be coupled to cellular activities that require energy.

 

Image: The ATP/ADP Reaction Cycle. Image credit: Shutterstock

ATP Production and Transport

The enzyme complex ATP synthase, located in the mitochondrial inner membrane, generates ATP from ADP and inorganic phosphate, using a proton gradient generated by the flow of electrons through the electron transport chain. As ATP synthase generates ATP, it deposits this molecule in the innermost region of the mitochondria (called the matrix or the lumen).

In order for ATP to become available to power cellular processes, it has to be transported out of the lumen and across the mitochondrial inner membrane into the cytoplasm. Unfortunately, the inner mitochondrial membrane is impermeable to ATP (and ADP). In order to overcome this barrier, a protein embedded in the inner membrane called ATP/ADP translocase performs the transport operation. Conveniently, for every molecule of ATP transported out of the lumen, a molecule of ADP is transported from the cytoplasm into the lumen. In turn, this ADP is converted into ATP by ATP synthase.

Because of the importance of this process, copies of ATP/ADP translocase comprises 10% of the proteins in the inner membrane.

If this enzyme doesn’t function properly, it will result in mitochondrial myopathies.

The Problem ATP Transport Causes for The Endosymbiont Hypothesis

Two intertwined questions confronting the endosymbiont hypothesis relate to the evolutionary driving force behind symbiogenesis and the nature of pre-mitochondria.

Traditionally, evolutionary biologists have posited that the host cell was an anaerobe, while the endosymbiont was an aerobic microbe, producing ATP from lactic acid generated by the host cell. (Lactic acid is the breakdown product of glucose in the absence of oxygen).

But, as cell biologist Franklin Harold points out, this scenario has an inherent flaw. Namely, if the endosymbiont is producing ATP necessary for its survival from host cell nutrients, why would it relinquish some—or even all—of the ATP it produces to the host cell?

According to Harold, “The trouble is that unless the invaders share their bounty with the host, they will quickly outgrow him; they would be pathogens, not symbionts.”²

And, the only way they could share their bounty with the host cell is to transport ATP from the engulfed cell’s interior to the host cell’s cytoplasm. While mitochondria accomplish this task with the ATP/ADP translocase, there is no good reason to think that the engulfed cell would do this. Given the role ATP plays as the energy currency in the cell and the energy that is expended to make this molecule, there is no advantage for the engulfed cell to pump ATP from its interior to the exterior environment.

Harold sums up the problem this way: “Such a carrier would not have been present in the free-living symbiont but must have been acquired in the course of its enslavement; it cannot be called upon to explain the initial benefits of the association.”³

In other words, currently, there is no evolutionary explanation for why the ATP/ADP translocase in the mitochondrial inner membrane—a protein central to the role of mitochondria in eukaryotic cells—pumps ATP from the lumen to the cytoplasm.

Two Alternative Models

This problem has led evolutionary biologists to propose two alternative models to account for the evolutionary driving force behind symbiogenesis: 1) the hydrogen hypothesis; and 2) the oxygen scavenger hypothesis.

The hydrogen hypothesis argues that the host cell was a methanogenic member of archaea that consumed hydrogen gas and the symbiont was a hydrogen-generating alpha proteobacteria.

The oxygen-scavenging model suggests that the engulfed cell was aerobic, and because it used oxygen, it reduced the amount of oxygen in the cytoplasm of the host cell, thought to be an anaerobe.

Today, most evolutionary biologists prefer the hydrogen hypothesis—in part because the oxygen scavenger model, too, has a fatal flaw. As Harold points out, “This [oxygen scavenger model], too, is dubious, because respiration generates free radicals that are known to be a major source of damage to cellular membranes and genes.”⁴

Moving Forward, Or Moving Backward?

To help make headway, two researchers from UVA attempted to reconstruct the evolutionary precursor to mitochondria, dubbed pre-mitochondria.

Operating within the evolutionary framework, these two investigators reconstructed the putative genome of pre-mitochondria using genes in the mitochondrial genome and genes from the nuclear genomes of organisms they believe were transferred to the nucleus during the process of symbiogenesis. (Genes that clustered with alphaproteobacterial genes were deemed to be of mitochondrial origin.)

Based on their reconstruction, they conclude that the original engulfed cell actually used its ATP/ADP translocase to import ATP from the host cell cytoplasm into its interior, exchanging the ATP for an ADP. This is the type of ATP/ADP translocase found in obligate intracellular parasites alive today.

According to the authors, this means that:

“Pre-mitochondrion [was] an ‘energy scavenger’ and suggests an energy parasitism between the endosymbiont and its host at the origin of the mitochondria. . . . This is in sharp contrast with the current role of mitochondria as the cell’s energy producer and contradicts the traditional endosymbiotic theory that the symbiosis was driven by the symbiont supplying the host ATP.”⁵

The authors speculate that at some point during symbiogenesis the ATP/ADP translocase “went ahead and backed up,” reversing direction. But, this explanation is little more than a just-so story with no evidential support. Confounding their conjecture is their discovery that the ATP/ADP translocase found in mitochondria is evolutionarily unrelated to the ATP/ADP translocases found in obligate intracellular parasites.

The fact that the engulfed cell was an obligate intracellular parasite not only brings a halt to the traditional version of the endosymbiont hypothesis, it flattens the tires of both the oxygen scavenger model and hydrogen hypothesis. According to Wang and Wu (the UVA investigators):

“Our results suggest that mitochondria most likely originated from an obligate intracellular parasite and not from a free-living bacterium. This has important implications for our understanding of the origin of mitochondria. It implies that at the beginning of the endosymbiosis, the bacterial symbiont provided no benefits whatsoever to the host. Therefore we argue that the benefits proposed by various hypotheses (e.g, oxygen scavenger and hydrogen hypotheses) are irrelevant in explaining the establishment of the initial symbiosis.”⁶

If the results of the analysis by the UVA researchers stand, it leaves evolutionary biologists with no clear direction when it comes to determining the evolutionary driving force behind the early stages of symbiogenesis or the evolutionary route to mitochondria.

It seems that the more evolutionary biologists probe the question of mitochondrial origins, the more confusion and uncertainty results. In fact, there is not a coherent compelling evolutionary explanation for the origin of eukaryotic cells—one of the key events in life’s history. The study by the UVA investigators (along with other studies) casts aspersions on the most prominent evolutionary explanations for the origin of eukaryotes, justifying skepticism about the grand claim of the evolutionary paradigm: namely, that the origin, design, and history of life can be explained exclusively through evolutionary processes.

In light of this uncertainty, can the origin of mitochondria, and hence eukaryotic cells, be better explained by a creation model? I think so, but for many scientists this is a road less traveled.

Resources

Challenges to the Endosymbiont Hypothesis:

• “Evolutionary Paradigm Lacks Explanation for Origin of Mitochondria and Eukaryotic Cells” by Fazale Rana (article)
• “Endosymbiont Hypothesis: Things Aren’t What They Seem to Be” by Fazale Rana (article)
• “Complex Protein Biogenesis Hints at Intelligent Design” by Fazale Rana (article)
• “Membrane Biochemistry Challenges Route to Evolutionary Origin of Complex Cells” by Fazale Rana (article)

In Support of a Creation Model for the Origin of Eukaryotic Cells:

• “Why Do Mitochondria Have DNA?” by Fazale Rana (article)
• “Mitochondrial Genomes: Evidence for Evolution or Creation?” by Fazale Rana (article)
• “Mitochondria’s Deviant Genetic Code: Creation or Evolution?” by Fazale Rana (article)
• “Can a Creation Model Explain the Origin of Mitochondria?” by Fazale Rana (article)
• “Why Mitochondria Make My List of Best Biological Designs” by Fazale Rana (article)

ATP Production and the Case for a Creator:

• “Molecular Logic of the Electron Transport Chain Supports Creation” by Fazale Rana (article)
• “Electron Transport Chain Protein Complexes Rev Up the Case for a Creator” by Fazale Rana (article)
• “ATP Synthase Ratchets up the Case for Intelligent Design” by Fazale Rana (article)
• “Addressing the Concerns of a Critic and the Case for Intelligent Design” by Fazale Rana (article)

If you find yourself in need of directions when traveling through New England and you ask a local for help, he or she just might reply, “You can’t get there from here.” As you can imagine, these aren’t welcome words, particularly when all you want to do is make your way to your destination.

Unfortunately, the same thing could be said to biologists trying to discover the evolutionary route that led to the emergence of complex, eukaryotic cells. No matter the starting point, it seems as if you just can’t get there from here.

This frustration becomes most evident as evolutionary biologists try to account for the biochemical makeup of the membranes found in eukaryotic cells. In my opinion, this struggle is not just an inconvenient detour. As the following paragraphs show, obstacles line the roadway, ultimately leading to a dead end that exposes the shortcomings of the endosymbiont hypothesis—a cornerstone idea in evolutionary biology.

Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis stands as the best explanation for the origin of complex cells. According to this hypothesis, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe.

The mitochondrion represents the “poster child” of the endosymbiont hypothesis. Presumably, this organelle started as an endosymbiont. Evolutionary biologists believe that once engulfed by the host cell, the microbe took up permanent residency, growing and dividing inside the host. Over time, the endosymbiont and host became mutually interdependent, with the endosymbiont providing a metabolic benefit—such as a source of ATP—for the host cell. In turn, the host cell provided nutrients to the endosymbiont. Presumably, the endosymbiont gradually evolved into an organelle through a process referred to as genome reduction. This reduction resulted when genes from the endosymbiont’s genome were transferred into the genome of the host organism.

Evidence for the Endosymbiont Hypothesis
1. Most of the evidence for the endosymbiont hypothesis centers around mitochondria and their similarity to bacteria. Mitochondria are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

2. Biochemical evidence also exists for the endosymbiont hypothesis. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. They see the biochemical similarities between mitochondrial and bacterial genomes as further evidence for the evolutionary origin of these organelles.

3. The presence of the unique lipid, cardiolipin, in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. This important lipid component of bacterial inner membranes is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider it a signature lipid for mitochondria and a vestige of the organelle’s evolutionary history. So far, the evolutionary route looks well-paved and clear.

Discovery of Lokiarchaeota

Evolutionary biologists have also developed other lines of evidence in support of the endosymbiont hypothesis. For example, biochemists have discovered that the genetic core (DNA replication and the transcription and translation of genetic information) of eukaryotic cells resembles that of the archaea. This similarity suggests to many biologists that a microbe belonging to the archaeal domain served as the host cell that gave rise to eukaryotic cells.

Life scientists think they may have determined the identity of that archaeal host. In 2015, a large international team of collaborators reported the discovery of Lokiarchaeota, a new phylum belonging to the archaea. This phylum clusters with eukaryotes on the evolutionary tree. Analysis of the genomes of Lokiarchaeota identifies a number of genes involved in membrane-related activities, suggesting that this microbe may well have possessed the ability to engulf other microbes.¹ At this point, it looks like “you can get there from here.”

Challenges to the Endosymbiont Hypothesis

Despite this seemingly compelling evidence, the evolutionary route to the first eukaryotic cells is littered with potholes. I have written several articles detailing some of the obstacles. (See Challenges to the Endosymbiont Hypothesis in the Resources section.) Also, a divide on the evolutionary roadway called the lipid divide compounds the problem for the endosymbiont hypothesis.

Lipid Divide

The lipid divide refers to the difference in the chemical composition of the cell membranes found in bacteria and archaea. Phospholipids comprise the cell membranes of both sorts of microbes. But the similarity ends there. The chemical makeup of the phospholipids is distinct in bacteria and archaea.

Bacterial phospholipids are built around a d-glycerol backbone, which has a phosphate moiety bound to the glycerol in the sn-3 position. Two fatty acids are bound to the d-glycerol backbone at the sn-1 and sn-2 positions. In water, these phospholipids assemble into bilayer structures.

Figure: Difference between archaeal (top) and bacterial (middle and bottom) phospholipids. Features include 1: isoprene chains, 2: ether linkage, 3: l-glycerol, 4 and 8: phosphate group, 5: fatty acid chains, 6: ester linkages, 7: d-glycerol, 9: lipid bilayer of bacterial membranes, 10: lipid monolayer found in some archaea. Image credit: Wikipedia

Archaeal phospholipids are constructed around an l-glycerol backbone (which produces membrane lipids with different stereochemistry than bacterial phospholipids). The phosphate moiety is attached to the sn-1 position of glycerol. Two isoprene chains are bound to the sn-2 and sn-3 positions of l-glycerol via ether linkages. Some archaeal membranes are formed from phospholipid bilayers, while others are formed from phospholipid monolayers.

Presumably, the structural features of the archaeal phospholipids serve as an adaptation that renders them ideally suited to form stable membranes in the physically and chemically harsh environments in which many archaea find themselves.

Lipid Divide Frustrates the Origin of Eukaryotic Cell Membranes

In light of the lipid divide and the evidence that seemingly indicates that the endosymbiotic host cell likely belonged to Lokiarchaeota, it logically follows that the membrane composition of eukaryotic cells should be archaeal-like. But, this expectation is not met and the evolutionary route encounters another pothole. Instead, the cell membranes of eukaryotic cells closely resemble bacterial membranes.

One way to repair the roadway is to posit that during the evolutionary process that led to the emergence of eukaryotic cells, a transition from archaeal-like membranes to bacterial-like membranes took place. In fact, supporting evidence comes from laboratory studies demonstrating that stable bilayers can form from a mixture of bacterial and archaeal phospholipids, even though the lipids from the two sources have opposite stereochemistry.

Evolutionary biologists Purificación López-García and David Moreira question if evidence can be marshaled in support of this scenario for two reasons.² First, mixing of phospholipids in the lab is a poor model for cell membranes that function as a “dynamic cell-environment interface.”³

Second, they question if this transition is feasible given how exquisitely optimized membrane proteins must be to fit into cell membranes. The nature of protein optimization is radically different for bacterial and archaeal membranes. Because cell membrane systems are optimized, the researchers question if an adequate driving force for this transition exists.

In other words, these two scientists express serious doubts about the biochemical viability of a transitional stage between archaeal membranes. In light of these obstacles, López-García and Moreira write, “The archaea-to-bacteria membrane shift remains the Achilles’ heel for these models [that propose an archaeal host for endosymbionts].”⁴

In other words, you can’t get there from here.

Can Lokiarchaeota Traverse the Lipid Divide?

In the midst of this uncertain evolutionary route, a recent study by investigators from the Netherlands seems to point the way toward the evolutionary origin of eukaryotic membranes.⁵ Researchers screened the Lokiarchaeota genome for enzymes that would take part in phospholipid synthesis with the hope of finding clues about how this transition may have occurred. They conclude that this group of microbes could not make l-glycerol-1-phosphate (a key metabolic intermediate in the production of archaeal phospholipids) because it lacked the enzyme glycerol-1-phosphate dehydrogenase (G1PDH). They also discovered evidence that suggests that this group of microbes could make fatty acids and chemically attach them to sugars. The researchers argue that Lokiarchaeota could make some type of hybrid phospholipid with features of both archaeal and bacterial phospholipids.

The team’s approach to understanding how evolutionary processes could bridge the lipid divide and account for the origin of eukaryotic membranes is clever and inventive, to be sure. But it is far from convincing for at least four reasons.

1. Absence of evidence is not evidence of absence, as the old saying goes. Just because the research team didn’t find the gene for G1PDH in the Lokiarchaeota genetic material doesn’t mean this microbe didn’t have the capacity to make archaeal-type phospholipids. Toward this end, it is important to note that researchers have not cultured any microbe that belongs to this group organisms. The group’s existence is inferred from metagenomic analysis, which involves isolating small fragments of DNA from the environment (in this case a hydrothermal vent system in the Atlantic Ocean, called Loki’s Castle) and stitching them together into a genome. The Lokiarchaeota “genome” is low quality (1.4-fold coverage) and incomplete (8 percent of the genome is missing). Around one-third (32 percent) of the genome codes for proteins with unknown function. Could it be that an enzyme capable of generating l-glycerol-1-phosphate exists in the mysterious third of the genome? Or in the missing 8 percent?

2. While the researchers discovered that genes could conceivably work together to make d-glycerol-3-phosphate (though the enzymes encoded by these genes perform different metabolic functions), they found no direct evidence that Lokiarchaeota produces d-glycerol-3-phosphate. Nor did they find evidence for glycerol-3-phosphate dehydrogenase (G3PDH) in the Lokiarchaeota genetic material. This enzyme plays a key role in the synthesis of phospholipids in bacteria.

3. Though the researchers found evidence that Lokiarchaeota had the capacity to make fatty acids, some of the genes required for the process seem to have been acquired by these microbes via horizontal gene transfer with genetic material from bacteria. (It should be noted that 29 percent of the Lokiarchaeota genome comes from the bacteria.) It is not clear when Lokiarchaeota acquired these genes and, therefore, if this metabolic capability has any bearing on the origin of eukaryotes.

4. The researchers present no evidence that Lokiarchaeota possessed the protein machinery that would chemically attach isoprenoid lipids to d-glycerol-3-phosphate via ether linkages.

Thus, the only way to establish Lokiarchaeota membranes as a transitional evolutionary pathway between those found in Archaea and Bacteria is to perform chemical analysis of its membranes. At this juncture, such analysis is impossible to perform because no one has been able to culture Lokiarchaeota. In fact, other evidence suggests that this group of microbes possessed archaeal-type membranes. Researchers have recovered archaeal lipids in the sediments surrounding Loki’s Castle, but they have not recovered bacterial-like lipids.

More Lipid Divide Frustration

Given these problems, could it be that the host microbe for the endosymbiont was a member of Bacteria, not Archaea? While this model would solve the problem of the lipid divide, it leaves unexplained the similarity between the genetic core of eukaryotes and the Archaea. Nor does it account for the grouping of eukaryotes with the Archaea.

It doesn’t look like you can get there from here, either.

Evolutionary biologists Jonathan Lombard, Purificación López-García and David Moreira sum things up when they write, “The origin of eukaryotic membranes is a problem that is rarely addressed by the different hypotheses that have been proposed to explain the emergence of eukaryotes.”⁶ Yet, until this problem is adequately addressed, the evolutionary route to eukaryotes will remain obscure and the endosymbiont hypothesis noncompelling.

In light of this challenge and others, maybe a better way to make sense of the origin of eukaryotic cells is to view them as the Creator’s handiwork. For many scientists, it is a road less traveled, but it accounts for all of the data. You can get there from here.

Resources

Challenges to the Endosymbiont Hypothesis

• “Evolutionary Paradigm Lacks Explanation for Origin of Mitochondria and Eukaryotic Cells” by Fazale Rana (article)
• “Complex Protein Biogenesis Hints at Intelligent Design” by Fazale Rana (article)
• “Endosymbiont Hypothesis: Things Aren’t What They Seem to Be” by Fazale Rana (article)

Support for a Creation Model for the Origin of Eukaryotic Cells

• “Why Do Mitochondria Have DNA?” by Fazale Rana (article)
• “Mitochondrial Genomes: Evidence for Evolution or Creation?” by Fazale Rana (article)
• “Mitochondria’s Deviant Genetic Code: Creation or Evolution?” by Fazale Rana (article)
• “Can a Creation Model Explain the Origin of Mitochondria?” by Fazale Rana (article)
• “Molecular Logic of the Electron Transport Chain Supports Creation” by Fazale Rana (article)
• “Why Mitochondria Make My List of Best Biological Designs” by Fazale Rana (article)

It was one of the most painful experiences I ever had. A few years ago, I had two back-to-back bouts of kidney stones. I remember it as if it were yesterday. Man, did it hurt when I passed the stones! All I wanted was for the emergency room nurse to keep the Demerol coming.

Figure 1: Schematic Depiction of Kidney Stones Moving through the Urinary Tract. Image Credit: Shutterstock

When all that misery was going down, I wished I was one of those rare individuals who doesn’t experience pain. There are some people who, due to genetic mutations, live pain-free lives. This condition is called hypoalgesia. (Of course, there is a serious downside to hypoalgesia. Pain lets us know when our body is hurt or sick. Because hypoalgesics can’t experience pain, they are prone to serious injury, etc.)

Biomedical researchers possess a keen interest in studying people with hypoalgesia. Identifying the mutations responsible for this genetic condition helps investigators understand the physiological processes that undergird the pain sensation. This insight then becomes indispensable to guiding efforts to develop new drugs and techniques to treat pain.

By studying the genetic profile of a 66-year-old woman who lived a lifetime with pain-free injuries, a research team from the UK recently discovered a novel genetic mutation that causes hypoalgesia.¹ The mutation responsible for this patient’s hypoalgesia occurred in a pseudogene, a region of the genome considered nonfunctional “junk DNA.”

This discovery adds to the mounting evidence that shows junk DNA is functional. At this point, molecular geneticists have demonstrated that virtually every class of junk DNA has function. This notion undermines the best evidence for common descent and, hence, undermines an evolutionary interpretation of biology. More importantly, the discovery adds support for the competitive endogenous RNA hypothesis, which can be marshaled to support RTB’s genomics model. It is becoming more and more evident to me that genome structure and function reflect the handiwork of a Creator.

The Role of a Pseudogene in Mediating Hypoalgesia

To identify the genetic mutation responsible for the 66-year-old’s hypoalgesia, the research team scanned her DNA along with samples taken from her mother and two children. The team discovered two genetic changes: (1) mutations to the FAAH gene that reduced its expression, and (2) deletion of part of the FAAH pseudogene.

The FAAH gene encodes for a protein called fatty acid amide hydrolase (FAAH). This protein breaks down fatty acid amides. Some of these compounds interact with cannabinoid receptors. These receptors are located in the membranes of cells found in tissues throughout the body. They mediate pain sensation, among other things. When fatty acid amide concentrations become elevated in the circulatory system, it produces an analgesic effect.

Researchers found elevated fatty acid amide levels in the patient’s blood, consistent with reduced expression of the FAAH gene. It appears that both mutations are required for the complete hypoalgesia observed in the patient. The patient’s mother, daughter, and son all display only partial hypoalgesia. The mother and daughter have the same mutation in the FAAH gene but an intact FAAH pseudogene. The patient’s son is missing the FAAH pseudogene, but has a “normal” FAAH gene.

Based on the data, it looks like proper expression levels of the FAAH gene require an intact FAAH pseudogene. This is not the first time that biomedical researchers have observed the same effect. There are a number of gene-pseudogene pairs in which both must be intact and transcribed for the gene to be expressed properly. In 2011, researchers from Harvard University proposed that the competitive endogenous RNA hypothesis explains why transcribed pseudogenes are so important for gene expression.²

The Competitive Endogenous RNA Hypothesis

Biochemists and molecular biologists have long believed that the primary mechanism for regulating gene expression centered around controlling the frequency and amount of mRNA produced during transcription. For housekeeping genes, mRNA is produced continually, while for genes that specify situational proteins, it is produced as needed. Greater amounts of mRNA are produced for genes expressed at high levels and limited amounts for genes expressed at low levels.

Researchers long thought that once the mRNA was produced it would be translated into proteins, but recent discoveries indicate this is not the case. Instead, an elaborate mechanism exists that selectively degrades mRNA transcripts before they can be used to direct the protein production at the ribosome. This mechanism dictates the amount of protein produced by permitting or preventing mRNA from being translated. The selective degradation of mRNA also plays a role in gene expression, functioning in a complementary manner to the transcriptional control of gene expression.

Another class of RNA molecules, called microRNAs, mediates the selective degradation of mRNA. In the early 2000s, biochemists recognized that by binding to mRNA (in the 3′ untranslated region of the transcript), microRNAs play a crucial role in gene regulation. Through binding, microRNAs flag the mRNA for destruction by RNA-induced silencing complex (RISC).

Figure 2: Schematic of the RNA-Induced Silencing Mechanism. Image Credit: Wikipedia

Various distinct microRNA species in the cell bind to specific sites in the 3′ untranslated region of mRNA transcripts. (These binding locations are called microRNA response elements.) The selective binding by the population of microRNAs explains the role that duplicated pseudogenes play in regulating gene expression.

The sequence similarity between the duplicated pseudogene and the corresponding “intact” gene means that the same microRNAs will bind to both mRNA transcripts. (It is interesting to note that most duplicated pseudogenes are transcribed.) When microRNAs bind to the transcript of the duplicated pseudogene, it allows the transcript of the “intact” gene to escape degradation. In other words, the transcript of the duplicated pseudogene is a decoy. The mRNA transcript can then be translated and, hence, the “intact” gene expressed.

It is not just “intact” and duplicated pseudogenes that harbor the same microRNA response elements. Other genes share the same set of microRNA response elements in the 3′ untranslated region of the transcripts and, consequently, will bind the same set of microRNAs. These genes form a network that, when transcribed, will influence the expression of all genes in the network. This relationship means that all the mRNA transcripts in the network can function as decoys. This recognition accounts for the functional utility of unitary pseudogenes.

One important consequence of this hypothesis is that mRNA has dual functions inside the cell. First, it encodes information needed to make proteins. Second, it helps regulate the expression of other transcripts that are part of its network.

Junk DNA and the Case for Creation

Evolutionary biologists have long maintained that identical (or nearly identical) pseudogene sequences found in corresponding locations in genomes of organisms that naturally group together (such as humans and the great apes) provide compelling evidence for shared ancestry. This interpretation was persuasive because molecular geneticists regarded pseudogenes as nonfunctional, junk DNA. Presumably, random biochemical events transformed functional DNA sequences (genes) into nonfunctional garbage.

Creationists and intelligent design proponents had little to offer by way of evidence for the intentional design of genomes. But all this changed with the discovery that virtually every class of junk DNA has function, including all three types of pseudogenes (processed, duplicated, and unitary).

If junk DNA is functional, then the sequences previously thought to show common descent could be understood as shared designs. The competitive endogenous RNA hypothesis supports this interpretation. This model provides an elegant rationale for the structural similarity between gene-pseudogene pairs and also makes sense of the widespread presence of unitary pseudogenes in genomes.

Of course, this insight also supports the RTB genomics model. And that sure feels good to me.

Resources

• Who Was Adam? A Creation Model Approach to the Origin of Humanity
• The Cell’s Design: How Chemistry Reveals the Creator’s Artistry
• “Pseudogene Decoy Reveal Hidden Evidence for Design” by Fazale Rana (article)
• “Functional Pseudogenes Are Everywhere!” by Fazale Rana (article)
• “High Levels of Pseudogene Expression Help Silence the Case for Common Descent” by Fazale Rana (article)
• “Scientific Upset: More Functions for Pseudogenes” by Fazale Rana (article)
• “Unitary Pseudogenes Have Function! Part 1” by Fazale Rana (article)
• “Unitary Pseudogenes Have Function! Part 2” by Fazale Rana (article)
• “Does the Evolutionary Paradigm Stymie Scientific Advance?” by Fazale Rana (article)
• “Evolution’s Flawed Approach to Science” by Fazale Rana (article)

Gregg Allman fronted the Allman Brothers Band for over 40 years until his death in 2017 at the age of 69. Writer Mark Binelli described Allman’s voice as “a beautifully scarred blues howl, old beyond its years.”¹

A rock legend who helped pioneer southern rock, Allman was as well known for his chaotic, dysfunctional personal life as for his accomplishments as a musician. Allman struggled with drug abuse and addiction. He was also married six times, with each marriage ending in divorce and, at times, in a public spectacle.

In a 2009 interview with Binelli for Rolling Stone, Allman reflected on his failed marriages: “To tell you the truth, it’s my sixth marriage—I’m starting to think it’s me.”²

Allman isn’t the only one to have trouble with marriage. As it turns out, so do evolutionary biologists—but for different reasons than Greg Allman.

To be more exact, evolutionary biologists have made an unexpected discovery about the evolutionary origin of monogamy (a single mate for at least a season) in animals—an insight that raises questions about the evolutionary explanation. Based on recent work headed by a large research team of investigators from the University of Texas (UT), Austin, it looks like monogamy arose independently, multiple times, in animals. And these origin events were driven, in each instance, by the same genetic changes.³

In my view, this remarkable example of evolutionary convergence highlights one of the many limitations of evolutionary theory. It also contributes to my skepticism (and that of other intelligent design proponents/creationists) about the central claim of the evolutionary paradigm; namely, the origin, design, history, and diversity of life can be fully explained by evolutionary mechanisms.

At the same time, the independent origins of monogamy—driven by the same genetic changes—(as well as other examples of convergence) find a ready explanation within a creation model framework.

Historical Contingency

To appreciate why I believe this discovery is problematic for the evolutionary paradigm, it is necessary to consider the nature of evolutionary mechanisms. According to the evolutionary biologist Stephen Jay Gould (1941–2002), evolutionary transformations occur in a historically contingent manner.⁴ This means that the evolutionary process consists of an extended sequence of unpredictable, chance events. If any of these events were altered, it would send evolution down a different trajectory.

To help clarify this concept, Gould used the metaphor of “replaying life’s tape.” If one were to push the rewind button, erase life’s history, and then let the tape run again, the results would be completely different each time. In other words, the evolutionary process should not repeat itself. And rarely should it arrive at the same end point.

Gould based the concept of historical contingency on his understanding of the mechanisms that drive evolutionary change. Since the time of Gould’s original description of historical contingency, several studies have affirmed his view. (For descriptions of some representative studies, see the articles listed in the Resources section.) In other words, researchers have experimentally shown that the evolutionary process is, indeed, historically contingent.

A Failed Prediction of the Evolutionary Paradigm

Given historical contingency, it seems unlikely that distinct evolutionary pathways would lead to identical or nearly identical outcomes. Yet, when viewed from an evolutionary standpoint, it appears as if repeated evolutionary outcomes are a common occurrence throughout life’s history. This phenomenon—referred to as convergence—is widespread. Evolutionary biologists Simon Conway Morris and George McGhee point out in their respective books, Life’s Solution and Convergent Evolution, that identical evolutionary outcomes are a characteristic feature of the biological realm.⁵ Scientists see these repeated outcomes at the ecological, organismal, biochemical, and genetic levels. In fact, in my book The Cell’s Design, I describe 100 examples of convergence at the biochemical level.

In other words, biologists have made two contradictory observations within the evolutionary framework: (1) evolutionary processes are historically contingent and (2) evolutionary convergence is widespread. Since the publication of The Cell’s Design, many new examples of convergence have been unearthed, including the recent origin of monogamy discovery.

Convergent Origins of Monogamy

Working within the framework of the evolutionary paradigm, the UT research team sought to understand the evolutionary transition to monogamy. To achieve this insight, they compared the gene expression profiles in the neural tissues of reproductive males for closely related pairs of species, with one species displaying monogamous behavior and the other nonmonogamous reproduction.

The species pairs spanned the major vertebrate groups and included mice, voles, songbirds, frogs, and cichlids. From an evolutionary perspective, these organisms would have shared a common ancestor 450 million years ago.

Monogamous behavior is remarkably complex. It involves the formation of bonds between males and females, care of offspring by both parents, and increased territorial defense. Yet, the researchers discovered that in each instance of monogamy the gene expression profiles in the neural tissues of the monogamous species were identical and distinct from the gene expression patterns for their nonmonogamous counterparts. Specifically, they observed the same differences in gene expression for the same 24 genes. Interestingly, genes that played a role in neural development, cell-cell signaling, synaptic activity, learning and memory, and cognitive function displayed enhanced gene expression. Genes involved in gene transcription and AMPA receptor regulation were down-regulated.

So, how do the researchers account for this spectacular example of convergence? They conclude that a “universal transcriptomic mechanism” exists for monogamy and speculate that the gene modules needed for monogamous behavior already existed in the last common ancestor of vertebrates. When needed, these modules were independently recruited at different times in evolutionary history to yield monogamous species.

Yet, given the number of genes involved and the specific changes in gene expression needed to produce the complex behavior associated with monogamous reproduction, it seems unlikely that this transformation would happen a single time, let alone multiple times, in the exact same way. In fact, Rebecca Young, the lead author of the journal article detailing the UT research team’s work, notes that “Most people wouldn’t expect that across 450 million years, transitions to such complex behaviors would happen the same way every time.”⁶

So, is there another way to explain convergence?

Convergence and the Case for a Creator

Prior to Darwin (1809–1882), biologists referred to shared biological features found in organisms that cluster into disparate biological groups as analogies. (In an evolutionary framework, analogies are referred to as evolutionary convergences.) They viewed analogous systems as designs conceived by the Creator that were then physically manifested in the biological realm and distributed among unrelated organisms.

In light of this historical precedence, I interpret convergent features (analogies) as the handiwork of a Divine mind. The repeated origins of biological features equate to the repeated creations by an intelligent Agent who employs a common set of solutions to address a common set of problems facing unrelated organisms.

Thus, the idea of monogamous convergence seems to divorce itself from the evolutionary framework, but it makes for a solid marriage in a creation model framework.

Resources

• The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)
• “Repeatable Evolution or Repeated Creation?” by Fazale Rana (article)
• “Convergence: Evidence for a Single Creator” by Fazale Rana (article)
• “Like a Fish Out of Water: Why I’m Skeptical of the Evolutionary Paradigm” by Fazale Rana (article)
• “Believing Impossible Things: Convergent Origins of Functional Junk DNA Sequences” by Fazale Rana (article)
• “Is Junk DNA Evidence for Biological Evolution?” by Fazale Rana (article)
• “Historical Contingency and the Improbability of Protein Evolution, Part 1” by Fazale Rana (article)
• “Historical Contingency and the Improbability of Protein Evolution, Part 2” by Fazale Rana (article)
• “Inability to Repeat the Past Dooms Evolution” by Fazale Rana (article)

Nobody likes to be interrupted when they are talking. It feels disrespectful and can be frustrating. Interruptions derail the flow of a conversation.

The editors tell me that I need to interrupt this lead to provide a “tease” for what is to come. So, here goes: Interruptions happen in biochemical systems, too. Life scientists long thought that these interruptions disrupted the flow of biochemical information. But, it turns out these interruptions serve an important function, offering a rejoinder a common argument against intelligent design.

Now back to the lead.

Perhaps it is no surprise that some psychologists study interruptions¹ with the hope of discovering answers to questions such as:

• Why do people interrupt?
• Who is most likely to interrupt?
• Do we all perceive interruptions in the same way?

While there is still much to learn about the science of interruptions, psychologists have discovered that men interrupt more often than women. Ironically, men often view women who interrupt as ruder and less intelligent than men who interrupt during conversations.

Researchers have also found that a person’s cultural background influences the likelihood that he or she will interrupt during a discourse. Personality also plays a role. Some people are more sensitive to pauses in conversation and, therefore, find themselves interrupting more often than those who are less uncomfortable with periods of silence.

Psychologists have learned that not all interruptions are the same. Some people interrupt because they want the “floor.” These people are called intrusive interrupters. Cooperative interrupters help move the conversation along by agreeing with the speaker and finishing the speaker’s thoughts.

Interruptions are not confined to conversations. They are a part of life, including the biochemical operations that take place inside the cell.

In fact, biochemists have discovered that the information harbored in genes, which contains the instructions to build proteins—the workhorse molecules of the cell—experience interruptions in their coding sequences. These intrusive interruptions would disrupt the flow of information in the cell during the process of protein synthesis if the interrupting sequences weren’t removed by the cell’s machinery.

Molecular biologists have long viewed these genetic “interruptions” (called introns) as serving no useful purpose for the cell, with introns comprising a portion of the junk DNA found in the genomes of eukaryotic organisms. But it turns out that introns—like cooperative interruptions during a conversation—serve a useful purpose, according to the recent work of two independent teams of molecular biologists.

Introns Are Abundant

Noncoding regions within genes, introns consist of DNA sequences that interrupt the coding regions (called exons) of a gene. Introns are pervasive in genomes of eukaryotic organisms. For example, 90 percent of genes in mammals consists of introns, with an average of 8 per gene.

After the information stored in a gene is copied into messenger RNA, the intron sequences are excised, and the exons spliced together by a protein-RNA complex known as a spliceosome.

Figure 1: Drawing of pre-mRNA to mRNA. Image credit: Wikipedia

Molecular biologists have long wondered why eukaryotic genes would be riddled with introns. Introns seemingly make the structure and expression of eukaryotic genes unnecessarily complicated. What possible purpose could introns serve? Researchers also thought that once the introns were spliced out of the messenger RNA sequences, they were discarded as genetic debris.

Introns Serve a Functional Purpose

But recent work by two independent research teams from Sherbrooke University in Quebec, Canada, and MIT, respectively, indicates that molecular biologists have been wrong about introns. They have learned that once spliced from messenger RNA, these fragments play a role in helping cells respond to stress.

Both research teams studied baker’s yeast. One advantage of using yeast as a model organism relates to the relatively small number of introns (295) in its genome.

Figure 2: A depiction of baker’s yeast. Image credit: Shutterstock

Taking advantage of the limited number of introns in baker’s yeast, the team from Sherbrooke University created hundreds of yeast strains—each one missing just one of its introns. When grown under normal conditions with a ready supply of available nutrients, the strains missing a single intron grew normally—suggesting that introns aren’t of much importance. But when the researchers grew the yeast cells under conditions of food scarcity, the yeast with the deleted introns frequently died.²

The MIT team observed something similar. They noticed that during the stationary phase of growth (when nutrients become depleted, slowing down growth), introns spliced from RNA accumulated in the growth medium. The researchers deleted the specific introns that they found in the growth medium from the baker’s yeast genome and discovered that the resulting yeast strains struggled to survive under nutrient-poor conditions.³

At this point, it isn’t clear how introns help cells respond to stress caused by a lack of nutrients, but they have some clues. The Sherbrooke University team thinks that the spliced-out introns play a role in repressing the production of proteins that help form ribosomes. These biochemical machines manufacture proteins. Because protein synthesis requires building block materials and energy, during periods when nutrients are scarce, protein production slows down in cells. Ratcheting down protein synthesis impedes cell growth but affords them a better chance to survive a lack of nutrients. One way cells can achieve this objective is to stop making ribosomes.

The MIT team thinks that some spliced-out introns interact with spliceosomes, preventing them from splicing out other introns. When this disruption happens, it slows down protein synthesis.

Both research groups believe that in times when nutrients are abundant, the spliced-out introns are broken down by the cell’s machinery. But when nutrients are scarce, that condition triggers intron accumulation.

At this juncture, it isn’t clear if the two research teams have uncovered distinct mechanisms that work collaboratively to slow down protein production, or if they are observing facets of the same mechanism. Regardless, it is evident that introns display functional utility. It’s a surprising insight that has important ramifications for our understanding of the structure and function of genomes. This insight has potential biomedical utility and theological implications, as well.

Intron Function and the Case for Creation

Scientists who view biology through the lens of the evolutionary paradigm are quick to conclude that the genomes of organisms reflect the outworking of evolutionary history. Their perspective causes them to see the features of genomes, such as introns, as little more than the remnants of an unguided evolutionary process. Within this framework, there is no reason to think that any particular DNA sequence element, including introns, harbors function. In fact, many life scientists regard the “evolutionary vestiges” in the genome as junk DNA. This clearly has been the case for introns.

Yet, a growing body of data indicates that virtually every category of so-called junk DNA displays function. We can now add introns—cooperative interrupters—to the list. And based on the data on hand, we can make a strong case that most of the sequence elements in genomes possess functional utility.

Could it be that scientists really don’t understand the biology of genomes? Or maybe we have the wrong paradigm?

It seems to me that science is in the midst of a revolution in our understanding of genome structure and function. Instead of being a wasteland of evolutionary debris, most of the genome appears to be functional. And the architecture and operations of genomes appear to be far more elegant and sophisticated than anyone ever imagined—at least within the confines of the evolutionary paradigm.

But what if the genome is viewed from a creation model framework?

The elegance and sophistication of genomes are features that are increasingly coming into scientific view. And this is precisely what I would expect if genomes were the product of a Mind—the handiwork of a Creator.

Now that is a discovery worth talking about.

Resources

• Who Was Adam? A Creation Model Approach to the Origin of Humanity, 2nd exp. ed., by Fazale Rana with Hugh Ross (book)
• The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)
• “Gene Architecture Illuminates the Brilliance of Life’s Molecular Logic” by Fazale Rana (article)
• “Junk DNA Hot Spots Have Evolutionary Biologists Singing the Blues” by Fazale Rana (article)
• “A Couple of Tasty Morsels” by Fazale Rana (article)
• “Yet Another Genetic Difference between Humans and Chimpanzees” by Fazale Rana (article)
• “Ribosomes: Manufactured by Design, Part 1” by Fazale Rana (article)
• “Ribosomes: Manufactured by Design, Part 2” by Fazale Rana (article)
• “Evolution’s Flawed Approach to Science” by Fazale Rana (article)