What would you say is the most readily recognizable scientific icon? Is it DNA, a telescope, or maybe a test tube?

Figure 1: Scientific Icons. Image credit: Shutterstock

Marketing experts recognize the power of icons. When used well, icons prompt consumers to instantly identify a brand or product. They can also communicate a powerful message with a single glance.

Though many skeptics question if it’s science at all, the intelligent design movement has identified a powerful icon that communicates its message. Today, when most people see an image the bacterial flagellum they immediately think: Intelligent Design.

This massive protein complex powerfully communicates sophisticated engineering that could only come from an Intelligent Agent. And along these lines, it serves as a powerful piece of evidence for a Creator’s handiwork. Careful study of its molecular architecture and operation provides detailed evidence that an Intelligent Agent must be responsible for biochemical systems and, hence, the origin of life. And, as it turns out, the more we learn about the bacterial flagellum, the more evident it becomes that a Creator must have played a role in the origin and design of life—at least at the biochemical level—as new research from Japan illustrates.¹

The Bacterial Flagellum

This massive protein complex looks like a whip extending from the bacterial cell surface. Some bacteria have only a single flagellum, others possess several flagella. Rotation of the flagellum(a) allows the bacterial cell to navigate its environment in response to various chemical signals.

Figure 2: Typical Bacteria with Flagella. Image credit: Shutterstock

An ensemble of 30 to 40 different proteins makes up the typical bacterial flagellum. These proteins function in concert as a literal rotary motor. The flagellum’s components include a rotor, stator, drive shaft, bushing, universal joint, and propeller. It is essentially a molecular-sized electrical motor directly analogous to human-produced rotary motors. The rotation is powered by positively charged hydrogen ions flowing through the motor proteins embedded in the inner membrane.

Figure 3: The Bacterial Flagellum. Image credit: Wikipedia

The Bacterial Flagellum and the Revitalized Watchmaker Argument

Typically, when intelligent design proponents/creationists use the bacterial flagellum to make the case for a Creator, they focus the argument on its irreducibly complex nature. I prefer a different tact. I like to emphasize the eerie similarity between rotary motors created by human designers and nature’ bacterial flagella.

The bacterial flagellum is just one of a large number of protein complexes with machine-like attributes. (I devote an entire chapter to biomolecular machines in my book The Cell’s Design.) Collectively, these biomolecular machines can be deployed to revitalize the Watchmaker argument.

Popularized by William Paley in the eighteenth century, this argument states that as a watch requires a watchmaker, so too, life requires a Creator. Following Paley’s line of reasoning, a machine is emblematic of systems produced by intelligent agents. Biomolecular machines display the same attributes as human-crafted machines. Therefore, if the work of intelligent agents is necessary to explain the genesis of machines, shouldn’t the same be true for biochemical systems?

Skeptics inspired by atheist philosopher David Hume have challenged this simple, yet powerful, analogy. They argue that the analogy would be compelling only if there is a high degree of similarity between the objects that form the analogy. Skeptics have long argued that biochemical systems and machines are too dissimilar to make the Watchmaker argument work.

However, the striking similarity between the machine parts of the bacterial flagellum and human-made machines cause this objection to evaporate. New work on flagella by Japanese investigators lends yet more support to the Watchmaker analogy.

New Insights into the Structure and Function of the Flagellum’s Universal Joint

The flagellum’s universal joint (sometimes referred to as the hook) transfers the torque generated by the motor to the propeller. The research team wanted to develop a deeper understanding of the relationship between the molecular structure of the hook and how the structural features influence its function as a universal joint.

Comprised of nearly 100 copies (monomers) of a protein called FlgE, the hook is a curved, tube-like structure with a hollow interior. FlgE monomers stack on top of each other to form a protofilament. Eleven protofilaments organize to form the hook’s tube, with the long axis of the protofilament aligning to form the long axis of the hook.

Each FlgE monomer consists of three domains, called D0, D1, and D2. The researchers discovered that when the FlgE monomers stack to form a protofilament, the D0, D1, and D2 domains of each of the monomers align along the length of the protofilament to form three distinct regions in the hook. These layers have been labeled the tube layer, the mesh layer, and the spring layer.

During the rotation of the flagellum, the protofilaments experience compression and extension. The movement of the domains, which changes their spatial arrangement relative to one another, mediates the compression and extension. These domain movements allow the hook to function as a universal joint that maintains a rigid tube shape against a twisting “force,” while concurrently transmitting torque from the motor to the flagellum’s filament as it bends along its axis.

Regardless of one’s worldview, it is hard not to marvel at the sophisticated and elegant design of the flagellum’s hook!

The Bacterial Flagellum and the Case for a Creator

If the Watchmaker argument holds validity, it seems reasonable to think that the more we learn about protein complexes, such as the bacterial flagellum, the more machine-like they should appear to be. This work by the Japanese biochemists bears out this assumption. The more we characterize biomolecular machines, the more reason we have to think that life stems from a Creator’s handiwork.

Dynamic properties of the hook assembly add to the Watchmaker argument (when applied to the bacterial flagellum). This structure is much more sophisticated and ingenious than the design of a typical universal joint crafted by human designers. This elegance and ingenuity of the hook are exactly the attributes I would expect if a Creator played a role in the origin and design of life.

Message received, loud and clear.

Resources

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

The Bacterial Flagellum and the Case for a Creator

• “The Provocative Case for Intelligent Design: New Discovery Highlights Machine-Like Character of the Bacterial Flagellum” by Fazale Rana (article)
• “Bacterial Flagellum Structure Stacks the Case for Intelligent Design” by Fazale Rana (article)
• “Manufacturing the Case for Intelligent Design” by Fazale Rana (article)
• “Increasing the Torque on Intelligent Design” by Fazale Rana (article)
• “Changing Gears” by David Rogstad (article)

Can Intelligent Design Be Part of the Scientific Construct?

• “Is SETI an Intelligent Design Program?” by Fazale Rana (article)
• “Can Science Detect the Creator’s Fingerprints in Nature?” by Fazale Rana (article)
• “Can Intelligent Design Be Part of the Construct of Science?” by Fazale Rana (article)

Cancer. Perhaps no other word evokes more fear, anger, and hopelessness.

It goes without saying that cancer is an insidious disease. People who get cancer often die way too early. And even though a cancer diagnosis is no longer an immediate death sentence—thanks to biomedical advances—there are still many forms of cancer that are difficult to manage, let alone effectively treat.

Cancer also causes quite a bit of consternation for those of us who use insights from science to make a case for a Creator. From my vantage point, one of the most compelling reasons to think that a Creator exists and played a role in the origin and design of life is the elegant, sophisticated, and ingenious designs of biochemical systems. And yet, when I share this evidence with skeptics—and even seekers—I am often met with resistance in the form of the question: What about cancer?

Why Would God Create a World Where Cancer Is Possible?

In effect, this question typifies one of the most common—and significant—objections to the design argument. If a Creator is responsible for the designs found in biochemistry, then why are so many biochemical systems seemingly flawed, inelegant, and poorly designed?

The challenge cancer presents for the design argument carries an added punch. It’s one thing to cite inefficiency of protein synthesis or the error-prone nature of the rubisco enzyme, but it’s quite another to describe the suffering of a loved one who died from cancer. There’s an emotional weight to the objection. These deaths feel horribly unjust.

Couldn’t a Creator design biochemistry so that a disease as horrific as cancer would never be possible—particularly if this Creator is all-powerful, all-knowing, and all-good?

I think it’s possible to present a good answer to the challenge that cancer (and other so-called bad designs) poses for the design argument. Recent insights published by a research duo from Cambridge University in the UK help make the case.¹

A Response to the Bad Designs in Biochemistry and Biology

Because the “bad designs” challenge is so significant (and so frequently expressed), I devoted an entire chapter in The Cell’s Design to addressing the apparent imperfections of biochemical systems. My goal in that chapter was to erect a framework that comprehensively addresses this pervasive problem for the design argument.

In the face of this challenge it is important to recognize that many so-called biochemical flaws are not genuine flaws at all. Instead, they arise as the consequences of trade-offs. In their cellular roles, many biochemical systems face two (or more) competing objectives. Effectively managing these opposing objectives means that it is impossible for every aspect of the system to perform at an optimal level. Some features must be carefully rendered suboptimal to ensure that the overall system performs robustly under a wide range of conditions.

Cancer falls into this category. It is not a consequence of flawed biochemical designs. Instead, cancer reflects a trade-off between DNA repair and cell survival.

DNA Damage and Cancer

The etiology (cause) of most cancers is complex. While about 10 percent of cancers have a hereditary basis, the vast proportion results from mutations to DNA caused by environmental factors.

Some of the damage to DNA stems from endogenous (internal) factors, such as water and oxygen in the cell. These materials cause hydrolysis and oxidative damage to DNA, respectively. Both types of damage can introduce mutations into this biomolecule. Exogenous chemicals (genotoxins) from the environment can also interact with DNA and cause damage leading to mutations. So does exposure to ultraviolet radiation and radioactivity from the environment.

Infectious agents such as viruses can also cause cancer. Again, these infectious agents cause genomic instability, which leads to DNA mutations.

Figure: Tumor Formation Process. Image credit: Shutterstock

In effect, DNA mutations are an inevitable consequence of the laws of nature, specifically the first and second laws of thermodynamics. These laws make possible the chemical structures and operations necessary for life to even exist. But, as a consequence, these same life-giving laws also undergird chemical and physical processes that damage DNA.

Fortunately, cells have the capacity to detect and repair damage to DNA. These DNA repair pathways are elaborate and sophisticated. They are the type of biochemical features that seem to support the case for a Creator. DNA repair pathways counteract the deleterious effects of DNA mutation by correcting the damage and preventing the onset of cancer.

Unfortunately, these DNA repair processes function incompletely. They fail to fully compensate for all of the damage that occurs to DNA. Consequently, over time, mutations accrue in DNA, leading to the onset of cancer. The inability of the cell’s machinery to repair all of the mutation-causing DNA damage and, ultimately, protect humans (and other animals) from cancer is precisely the thing that skeptics and seekers alike point to as evidence that counts against intelligent design.

Why would a Creator make a world where cancer is possible and then design cancer-preventing processes that are only partially effective?

Cancer: The Result of a Trade-Off

Even though mutations to DNA cause cancer, it is rare that a single mutation leads to the formation of a malignant cell type and, subsequently, tumor growth. Biomedical researchers have discovered that the onset of cancer involves a series of mutations to highly specific genes (dubbed cancer genes). The mutations that cause cells to transform into cancer cells are referred to as driver mutations. Researchers have also learned that most cells in the body harbor a vast number of mutations that have little or no biological consequence. These mutations are called passenger mutations. As it turns out, there are thousands of passenger mutations in a typical cancer cell and only about ten driver mutations to so-called cancer genes. Biomedical investigators have also learned that many normal cells harbor both passenger and driver mutations without ever transforming. (It appears that other factors unrelated to DNA mutation play a role in causing a cancer cell to undergo extensive clonal expansion, leading to the formation of a tumor.)

What this means is that mutations to DNA are quite extensive, even in normal, healthy cells. But this factor prompts the question: Why is the DNA repair process so lackluster?

The research duo from Cambridge University speculate that DNA repair is so costly to cells—making extensive use of energy and cell resources—that to maintain pristine genomes would compromise cell survival. These researchers conclude that “DNA quality control pathways are fully functional but naturally permissive of mutagenesis even in normal cells.”² And, it seems as if the permissiveness of the DNA repair processes generally have little consequence given that a vast proportion of the human genome consists of noncoding DNA.

Biomedical researchers have uncovered another interesting feature about the DNA repair processes. The processes are “biased,” with repairs taking place preferentially on the DNA strand (of the double helix) that codes for proteins and, hence, is transcribed. In other words, when DNA repair takes place it occurs where it counts the most. This bias displays an elegant molecular logic and rationale, strengthening the case for design.

Given that driver mutations are not in and of themselves sufficient to lead to tumor formation, the researchers conclude that cancer prevention pathways are quite impressive in the human body. They conclude, “Considering that an adult human has ~30 trillion cells, and only one cell develops into a cancer, human cells are remarkably robust at preventing cancer.”³

So, what about cancer?

Though cancer ravages the lives of so many people, it is not because of poorly designed, substandard biochemical systems. Given that we live in a universe that conforms to the laws of thermodynamics, cancer is inevitable. Despite this inevitability, organisms are designed to effectively ward off cancer.

Ironically, as we gain a better understanding of the process of oncogenesis (the development of tumors), we are uncovering more—not less—evidence for the remarkably elegant and ingenious designs of biochemical systems.

The insights by the research team from Cambridge University provide us with a cautionary lesson. We are often quick to declare a biochemical (or biological) feature as poorly designed based on incomplete understanding of the system. Yet, inevitably, as we learn more about the system we discover an exquisite rationale for why things are the way they are. Such knowledge is consistent with the idea that these systems stem from a Creator’s handiwork.

Still, this recognition does little to dampen the fear and frustration associated with a cancer diagnosis and the pain and suffering experienced by those who battle cancer (and their loved ones who stand on the sidelines watching the fight take place). But, whether we are a skeptic or a believer, we all should be encouraged by the latest insights developed by the Cambridge researchers. The more we understand about the cause and progression of cancers, the closer we are to one day finding cures to a disease that takes so much from us.

We can also take added encouragement from the powerful scientific case for a Creator’s existence. The Old and New Testaments teach us that the Creator revealed by scientific discovery has suffered on our behalf and will suffer alongside us—in the person of Christ—as we walk through the difficult circumstances of life.

Resources

• The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)
• “Q&A: Why Would a Limitless Creator Face Trade-Offs in Biochemical Designs?” by Fazale Rana (article)

Examples of Biochemical Trade-Offs

• “30 % Inefficiency by Design” by Fazale Rana (article)
• “Uprooting a “Bad Design” Argument” by Fazale Rana (article)
• “Does Inflammation after Injury Traumatize the Case for Intelligent Design?” by Fazale Rana (article)
• “Cars and Cells: How Trade-Offs Make Good Designs” by Fazale Rana (article)
• Reactive Oxygen Species: Harbingers of Evolution or Signals of Design?” by Fazale Rana (article)
• “DNA Replication Winds Up the Case for Intelligent Design” by Fazale Rana (article)

Evidence that Nonfunctional DNA Serves as a Mutational Buffer

• “New Research Suggests Two Overlooked Functions of Junk DNA” by Fazale Rana (article)
• “Is 75% of the Human Genome Junk DNA?” by Fazale Rana (article)

What would it be like to live in a world without antibiotics?

It isn’t that hard to imagine, because antibiotics weren’t readily available for medical use until after World War II. And since that time, widespread availability of antibiotics has revolutionized medicine. However, the ability to practice modern medicine is being threatened because of the rise of antibiotic-resistant bacteria. Currently, there exists a pressing need to understand the evolution of antibiotic-resistant strains and to develop new types of antibiotics. Surprisingly, this worthy pursuit has unwittingly stumbled upon evidence for a Creator’s role in the design of biochemical systems.

Alexander Fleming (1881–1955) discovered the first antibiotic, penicillin, in 1928. But it wasn’t until Ernst Chain, Howard Florey, and Edward Abraham purified penicillin in 1942 and Norman Heatley developed a bulk extraction technique in 1945 that the compound became available for routine medical use.

Figure 1: Alexander Fleming. Image Credit: Wikipedia

Prior to this time, people often died from bacterial infections. Complicating this vulnerability to microbial pathogens was the uncertain outcome of many medical procedures. For example, patients often died after surgery due to complications arising from infections.

Figure 2: A generalized structure for penicillin antibiotics. Image credit: Shutterstock

Bacterial Resistance Necessitates New Antibiotics

Unfortunately, because of the growing threat of superbugs—antibiotic-resistant strains of bacteria—health experts around the world worry that we soon will enter into a post-antibiotic era in which modern medicine will largely revert to pre-World War II practices. According to Dr. David Livermore, laboratory director at Public Health England, which is responsible for monitoring antibiotic-resistant strains of bacteria, “A lot of modern medicine would become impossible if we lost our ability to treat infections.”¹

Without antibiotics, people would routinely die of infections that we easily treat today. Abdominal surgeries would be incredibly risky. Organ transplants and chemotherapy would be out of the question. And the list continues.

The threat of entering into a post-antibiotic age highlights the desperate need to develop new types of antibiotics. It also highlights the need to develop a better understanding of evolutionary processes that lead to the emergence of antibiotic resistance in bacteria.

Recently, a research team from Michigan State University (MSU) published a report that offers insight into the latter concern. These researchers studied the evolution of antibiotic resistance in bacteria that had been serially cultured in the laboratory for multiple decades in media that was free from antibiotics.² Through this effort, they learned that the genetic history of the bacterial strain plays a key role in its acquisition of resistance to antibiotics.

This work has important implications for public health, but it also carries theological implications. The decades-long experiment provides evidence that the elegant designs characteristic of biochemical and biological systems most likely stem from a Creator’s handiwork.

The Long-Term Evolution Experiment

To gain insight into the role that genetic history plays in the evolution of antibiotic resistance, the MSU researchers piggy-backed on the famous Long-Term Evolution Experiment (LTEE) at Michigan State University. Inaugurated in 1988, the LTEE is designed to monitor evolutionary changes in the bacterium E. coli, with the objective of developing an understanding of the evolutionary process.

Figure 3: A depiction of E. coli. Image Credit: Shutterstock

The LTEE began with a single cell of E. coli that was used to generate twelve genetically identical lines of cells. The twelve clones of the parent E. coli cell were separately inoculated into a minimal growth medium containing low levels of glucose as the only carbon source. After growing overnight, an aliquot (equal fractional part) of each of the twelve cultures was transferred into fresh growth media. This process has been repeated every day for about thirty years. Throughout the experiment, aliquots of cells have been frozen every 500 generations. These frozen cells represent a “fossil record” of sorts that can be thawed out and compared to current and other past generations of cells.

Relaxed Selection and Decay of Antibiotic Resistance

In general, when a population of organisms no longer experiences natural selection for a particular set of traits (antibiotic resistance, in this case), the traits designed to handle that pressure may experience functional decay as a result of mutations and genetic drift. This process is called relaxed selection.

In the case of antibiotic resistance, when the threat of antibiotics is removed from the population (relaxed selection), it seems reasonable to think that antibiotic resistance would decline in the population because in most cases antibiotic resistance comes with a fitness cost. In other words, bacterial strains that acquire antibiotic resistance face a trade-off that makes them less fit in environments without the antibiotic.

Genetic History and the Re-Evolution of Antibiotic Resistance

In light of this expectation, the MSU researchers wondered how readily bacteria that have experienced relaxed selection can overcome loss of antibiotic resistance when the antibiotic is reintroduced to the population.

To explore this question, the researchers examined the evolution of antibiotic resistance in the LTEE ancestor by exposing it to a set of different antibiotics and compared its propensity to acquire antibiotic resistance with four strains of E. coli derived from the LTEE ancestor (that underwent 50,000 generations of daily growth and transfer into fresh media in the absence of exposure to antibiotics).

As expected, the MSU team discovered that 50,000 generations of relaxed selection rendered the four strains more susceptible to four different antibiotics (ampicillin, ceftriaxone, ciprofloxacin, and tetracycline) compared to the LTEE ancestor. When they exposed these strains to the different antibiotics, the researchers discovered that acquisition of antibiotic resistance was idiosyncratic: some strains more readily evolved antibiotic resistance than the LTEE ancestor and others were less evolvable.

Investigators explained this difference by arguing that during the period of relaxed selection some of the strains experienced mutations that constrained the evolution of antibiotic resistance, whereas others experienced mutations that potentiated (activated) the evolution of antibiotic resistance. That is, historical contingency has played a key role in the acquisition of antibiotic resistance. Different bacterial lineages accumulated genetic differences that influence their capacity to evolve and adapt in new directions.

Historical Contingency

This study follows on the heels of previous studies that demonstrate the historical contingency of the evolutionary process.³ In other words, chance governs biological and biochemical evolution at its most fundamental level. As the MSU researchers observed, evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection (or that experience relaxed selection), which, too, consists of chance components.

Because of the historically contingent nature of the evolutionary process, it is highly unlikely that the same biological and biochemical designs should appear repeatedly throughout nature. In his book Wonderful Life, Stephen Jay 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.⁴

The “Problem” of Convergence

And yet, we observe the opposite pattern in biology. From an evolutionary perspective, it appears as if the evolutionary process independently and repeatedly arrived at the same outcome, time and time again (convergence). As evolutionary biologists Simon Conway Morris and George McGhee point out in their respective books Life’s Solution and Convergent Evolution, identical evolutionary outcomes are a widespread feature of the biological realm.⁵

Scientists see these repeated outcomes at ecological, organismal, biochemical, and genetic levels. To illustrate the pervasiveness of convergence at the biochemical level, I describe 100 examples of convergence in my book The Cell’s Design.⁶

From my perspective, the widespread occurrence of convergent evolution is a feature of biology that evolutionary theory can’t genuinely explain. In fact, given the clear-cut demonstration that the evolutionary process is historically contingent, I see the widespread occurrence of convergence as a failed scientific prediction for the evolutionary paradigm.

 

Evolution in Bacteria Doesn’t Equate to Large-Scale Evolution

The evolution of E. coli in the LTEE doesn’t necessarily validate the evolutionary paradigm. Just because such change is observed in a microbe doesn’t mean that evolutionary processes can adequately account for life’s origin and history, and the full range of biodiversity.

 

Convergence and the Case for Creation

Instead of viewing convergent features as having emerged through repeated evolutionary outcomes, we could understand them as reflecting the work of a divine Mind. In this scheme, 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.

Sadly, many in the scientific community are hesitant to embrace this perspective because they are resistant to the idea that design and purpose may play a role in biology. But, one can hope that someday the scientific community will be willing to move into a post-evolution future as the evidence for a Creator’s role in biology mounts.

Resources

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

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)

Microbial Evolution and the Validity of the Evolutionary Paradigm

• “Do Plastic-Eating Bacteria Dump the Case for Creation?” by Fazale Rana (article)
• “Does the Evolution of Caffeine-Eating Bacteria Stimulate the Case for Biological Evolution?” by Fazale Rana (article)

Are you a Marvel or a DC fan?

Do you like the Marvel superheroes better than those who occupy the DC universe? Or is it the other way around for you?

Even though you might prefer DC over Marvel (or Marvel over DC), over the years these two comic book rivals have often created superheroes with nearly identical powers. In fact, a number of Marvel and DC superheroes are so strikingly similar that their likeness to one another is obviously intentional.¹

Here are just a few of the superheroes Marvel and DC have ripped off each other:

• Superman (DC, created in 1938) and Hyperion (Marvel, created in 1969)
• Batman (DC, created in 1939) and Moon Knight (Marvel, created in 1975)
• Green Lantern (DC, created in 1940) and Nova (Marvel, created in 1976)
• Catwoman (DC, created in 1940) and Black Cat (Marvel, created in 1979)
• Atom (DC, created in 1961) and Ant-Man (Marvel, created in 1962)
• Aquaman (DC, created in 1941) and Namor (Marvel, created in 1939)
• Green Arrow (DC, created in 1941) and Hawkeye (Marvel, created in 1964)
• Swamp Thing (DC, created in 1971) and Man Thing (Marvel, created in 1971)
• Deathstroke (DC, created in 1980) and Deadpool (Marvel, created in 1991)

This same type of striking similarity is also found in biology. Life scientists have discovered countless examples of biological designs that are virtually exact replicas of one another. Yet, these identical (or nearly identical) designs occur in organisms that belong to distinct, unrelated groups (such as the camera eyes of vertebrates and octopi). Therefore, they must have an independent origin.

 

Figure 1: The Camera Eyes of Vertebrates (left) and Cephalopods (right); 1: Retina; 2: Nerve Fibers; 3: Optic Nerve; 4: Blind Spot. Image credit: Wikipedia

From an evolutionary perspective, it appears as if the evolutionary process independently and repeatedly arrived at the same outcome, time and time again. As evolutionary biologists Simon Conway Morris and George McGhee point out in their respective books, Life’s Solution and Convergent Evolution, identical evolutionary outcomes are a widespread feature of the biological realm.2 Scientists observe these repeated outcomes (known as convergence) 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 genuinely explain. In fact, I see pervasive convergence as a failed scientific prediction—for the evolutionary paradigm. Recent work by a research team from Stanford University demonstrates my point.3

These researchers discovered that identical genetic changes occurred when: (1) bats and whales “evolved” echolocation, (2) killer whales and manatees “evolved” specialized skin in support of their aquatic lifestyles, and (3) pikas and alpacas “evolved” increased lung capacity required to live in high-altitude environments.

Why do I think this discovery is so problematic for the evolutionary paradigm? To understand my concern, we first need to consider the nature of the evolutionary process.

Biological Evolution Is Historically Contingent

Essentially, 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.

The concept of historical contingency embodies this idea and is the theme of Stephen Jay Gould’s book Wonderful Life.4 To help illustrate the concept, Gould uses 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.

Are Evolutionary Processes Historically Contingent?

Gould based the concept of historical contingency on his understanding of the evolutionary process. In the decades since Gould’s original description of historical contingency, several studies have affirmed his view.

For example, in a landmark study in 2002, two Canadian investigators simulated macroevolutionary processes using autonomously replicating computer programs, with the programs operating like digital organisms.5 These programs were placed into different “ecosystems” and, because they replicated autonomously, could evolve. By monitoring the long-term evolution of the 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.

The Origin of Echolocation

One of the most remarkable examples of convergence is the independent origin of echolocation (sound waves emitted from an organism to an object and then back to the organism) in bats (chiropterans) and cetaceans (toothed whales). Research indicates that echolocation arose independently in two different groups of bats and also in the toothed whales.

 

Figure 2: Echolocation in Bats. Image credit: Shutterstock

One reason why this example of convergence is so remarkable has to do with the way some evolutionary biologists account for the widespread occurrences of convergence in biological systems. Undaunted by the myriad examples of convergence, these scientists assert that independent evolutionary outcomes result when unrelated organisms encounter nearly identical selection forces (e.g., environmental, competitive, and predatory pressures). According to this idea, natural selection channels unrelated organisms down similar pathways toward the same endpoint.

But this explanation is unsatisfactory because bats and whales live in different types of habitats (terrestrial and aquatic). Consequently, the genetic changes responsible for the independent emergence of echolocation in the chiropterans and cetaceans should be distinct. Presumably, the evolutionary pathways that converged on a complex biological system such as echolocation would have taken different routes that would be reflected in the genomes. In other words, even though the physical traits appear to be identical (or nearly identical), the genetic makeup of the organisms should reflect an independent evolutionary history.

But this expectation isn’t borne out by the data.

Genetic Convergence Parallels Trait Convergence

In recent years, evolutionary biologists have developed interest in understanding the genetic basis for convergence. Specifically, these scientists want to understand the genetic changes that lead to convergent anatomical and physiological features (how genotype leads to phenotype).

Toward this end, a Stanford research team developed an algorithm that allowed them to search through entire genome sequences of animals to identify similar genetic features that contribute to particular biological traits.6 In turn, they applied this method to three test cases related to the convergence of:

• echolocation in bats and whales
• scaly skin in killer whales
• lung structure and capacity in pikas and alpacas

The investigators discovered that for echolocating animals, the same 25 convergent genetic changes took place in their genomes and were distributed among the same 18 genes. As it turns out, these genes play a role in the development of the cochlear ganglion, thought to be involved in echolocation. They also discovered that for aquatic mammals, there were 27 identical convergent genetic changes that occurred in same 15 genes that play a role in skin development. And finally, for high-altitude animals, they learned that the same 25 convergent genetic changes occurred in the same 16 genes that play a role in lung development.

In response to this finding, study author Gill Bejerano remarked, “These genes often control multiple functions in different tissues throughout the body, so it seems it would be very difficult to introduce even minor changes. But here we’ve found that not only do these very different species share specific genetic changes, but also that these changes occur in coding genes.”7

In other words, these results are not expected from an evolutionary standpoint. It is nothing short of amazing that genetic convergence would parallel phenotypic convergence.

On the other hand, these results make perfect sense from a creation model vantage point.

Convergence and the Case for Creation

Instead of viewing convergent features as having emerged through repeated evolutionary outcomes, we could understand them as reflecting the work of a Divine Mind. In this scheme, 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.

Like the superhero rip-offs in the Marvel and DC comics, the convergent features in biology appear to be intentional, reflecting a teleology that appears to be endemic in living systems.

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)
• “Convergence: Evidence for a Single Creator” by Fazale Rana (article)

The Historical Contingency of the Evolutionary Process

• “Inability to Repeat the 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)

I knew my career as a baseball player would be short-lived when, as a thirteen-year-old, I made the transition from Little League to the Babe Ruth League, which uses official Major League Baseball rules. Suddenly there were a whole lot more rules for me to follow than I ever had to think about in Little League.

Unlike in Little League, at the Babe Ruth level the hitter and base runners have to know what the other is going to do. Usually, the third-base coach is responsible for this communication. Before each pitch is thrown, the third-base coach uses a series of hand signs to relay instructions to the hitter and base runners.

Credit: Shutterstock

My inability to pick up the signs from the third-base coach was a harbinger for my doomed baseball career. I did okay when I was on base, but I struggled to pick up his signs when I was at bat.

The issue wasn’t that there were too many signs for me to memorize. I struggled recognizing the indicator sign.

To prevent the opposing team from stealing the signs, it is common for the third-base coach to use an indicator sign. Each time he relays instructions, the coach randomly runs through a series of signs. At some point in the sequence, the coach gives the indicator sign. When he does that, it means that the next signal is the actual sign.

All of this activity was simply too much for me to process. When I was at the plate, I couldn’t consistently keep up with the third-base coach. It got so bad that a couple of times the third-base coach had to call time-out and have me walk up the third-base line, so he could whisper to me what I was to do when I was at the plate. It was a bit humiliating.

Codes Come from Intelligent Agents

The signs relayed by a third-base coach to the hitter and base runners are a type of code—a set of rules used to convert and convey information across formats.

Experience teaches us that it takes intelligent agents, such as baseball coaches, to devise codes, even those that are rather basic in their design. The more sophisticated a code, the greater the level of ingenuity required to develop it.

Perhaps the most sophisticated codes of all are those that can detect errors during data transmission.

I sure could have used a code like that when I played baseball. It would have helped me if the hand signals used by the third-base coach were designed in such a way that I could always understand what he wanted, even if I failed to properly pick up the indicator signal.

The Genetic Code

As it turns out, just such a code exists in nature. It is one of the most sophisticated codes known to us—far more sophisticated than the best codes designed by the brightest computer engineers in the world. In fact, this code resides at the heart of biochemical systems. It is the genetic code.

This biochemical code consists of a set of rules that define the information stored in DNA. These rules specify the sequence of amino acids that the cell’s machinery uses to build proteins. In this process, information formatted as nucleotide sequences in DNA is converted into information formatted as amino acid sequences in proteins.

Moreover, the genetic code is universal, meaning that all life on Earth uses it.¹

Biochemists marvel at the design of the genetic code, in part because its structure displays exquisite optimization. This optimization includes the capacity to dramatically curtail errors that result from mutations.

Recently, a team from Germany identified another facet of the genetic code that is highly optimized, further highlighting its remarkable qualities.²

The Optimal Genetic Code

As I describe in The Cell’s Design, scientists from Princeton University and the University of Bath (UK) quantified the error-minimization capacity of the genetic code during the 1990s. Their work indicated that the universal genetic code is optimized to withstand the potentially harmful effects of substitution mutations better than virtually any other conceivable genetic code.³

In 2018, another team of researchers from Germany demonstrated that the universal genetic code is also optimized to withstand the harmful effects of frameshift mutations—again, better than other conceivable codes.⁴

In 2007, researchers from Israel showed that the genetic code is also optimized to harbor overlapping codes.⁵ This is important because, in addition to the genetic code, regions of DNA harbor other overlapping codes that direct the binding of histone proteins, transcription factors, and the machinery that splices genes after they have been transcribed.

The Robust Optimality of the Genetic Code

With these previous studies serving as a backdrop, the German research team wanted to probe more deeply into the genetic code’s optimality. These researchers focused on potential optimality of three properties of the genetic code: (1) resistance to harmful effects of substitution mutations, (2) resistance to harmful effects of frameshift mutations, and (3) capacity to support overlapping genes.

As with earlier studies, the team assessed the optimality of the naturally occurring genetic code by comparing its performance with sets of random codes that are conceivable alternatives. For all three property comparisons, they discovered that the natural (or standard) genetic code (SGC) displays a high degree of optimality. The researchers write, “We find that the SGC’s optimality is very robust, as no code set with no optimised properties is found. We therefore conclude that the optimality of the SGC is a robust feature across all evolutionary hypotheses.”⁶

On top of this insight, the research team adds one other dimension to multidimensional optimality of the genetic code: its capacity to support overlapping genes.

Interestingly, the researchers also note that the results of their work raise significant challenges to evolutionary explanations for the genetic code, pointing to the code’s multidimensional optimality that is extreme in all dimensions. They write:

We conclude that the optimality of the SGC is a robust feature and cannot be explained by any simple evolutionary hypothesis proposed so far. . . . the probability of finding the standard genetic code by chance is very low. Selection is not an omnipotent force, so this raises the question of whether a selection process could have found the SGC in the case of extreme code optimalities.⁷

While natural selection isn’t omnipotent, a transcendent Creator would be, and could account for the genetic code’s extreme optimality.

The Genetic Code and the Case for a Creator

In The Cell’s Design, I point out that our common experience teaches us that codes come from minds. It’s true on the baseball diamond and true in the computer lab. By analogy, the mere existence of the genetic code suggests that biochemical systems come from a Mind—a conclusion that gains additional support when we consider the code’s sophistication and exquisite optimization.

The genetic code’s ability to withstand errors that arise from substitution and frameshift mutations, along with its optimal capacity to harbor multiple overlapping codes and overlapping genes, seems to defy naturalistic explanation.

As a neophyte playing baseball, I could barely manage the simple code the third-base coach used. How mind-boggling it is for me when I think of the vastly superior ingenuity and sophistication of the universal genetic code.

And, just like the hitter and base runner work together to produce runs in baseball, the elegant design of the genetic code and the inability of evolutionary processes to account for its extreme multidimensional optimization combine to make the case that a Creator played a role in the origin and design of biochemical systems.

With respect to the case for a Creator, the insight from the German research team hits it out of the park.

Resources:

• The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)
• “FYI: ID in DNA” by Fazale Rana (article)
• “The Genetic Code: Simply the Best” by Fazale Rana (article)
• “The Optimal Design of the Genetic Code” by Fazale Rana (article)
• “Mitochondria’s Deviant Genetic Code: Evolution or Creation” by Fazale Rana (article)
• “Biochemical Synonyms Optimized, Part 1” by Fazale Rana (article)
• “Biochemical Synonyms Optimized, Part 2” by Fazale Rana (article)

I feel cold all the time.

When I was younger, I was always hot. I needed to be in air conditioning everywhere I went. I could never get the temperature cold enough. But now that I am older, I feel like a frail person who is always chilled, needing to drape myself with a blanket to keep warm.

Nevertheless, like all human beings, I am still warm-blooded. I am an endotherm, as are all mammals and birds.

For many biologists, endothermy represents a bit of an enigma. Maintaining a constant body temperature requires an elevated basal metabolic rate. But the energy needed to preserve a constant body temperature doesn’t come cheap. In fact, warm-blooded animals demand 30 times the energy per unit time compared to cold-blooded (ectothermic) creatures.

Though biologists have tried to account for endothermy, no model has adequately explained why birds and mammals are warm-blooded. The advantages of being warm-blooded over being cold-blooded have not seemed to adequately outweigh costs—until now.

Recently, a biologist from the University of Nevada, Reno, Michael L. Logan, published a model that helps make sense of this enigma.¹ His work evokes the optimal design and elegant rationale for endothermy in birds and mammals—and ectothermy in amphibians and reptiles.

An Explanation for Endothermy

For endothermy to exist, it must confer some significant advantage for animals’ constant, elevated body temperatures.

Logan argues that endothermy maintains mammalian and bird body temperatures close to the thermal optimum for immune system functionality. The operations of the immune system are temperature-dependent. If the temperature is too low or too high, the immune system responds poorly to infectious agents. But an elevated and stable body temperature primes mammalian and bird immune systems to rapidly and effectively respond to pathogens. When birds and mammals acquire a pathogen, their bodies mount a fever response. This slight elevation in temperature places their body temperature at the thermal optimum.

In other words, the fever response plays a critical role when animals battle infectious agents. And warm-blooded animals have the advantage of possessing body temperatures close to ideal.

Temperature and Immune System Function

A body of evidence indicates that the immune system’s components display temperature-dependent changes in activity. As it turns out, fever optimizes immune system function by:

1. Increasing the flow of blood through the bloodstream because of the vasodilation (blood vessel expansion) associated with fever. This increased blood flow accelerates the movement of immune cells throughout the body, giving them more timely access to pathogens.
2. Increasing binding of immune system proteins to immune cells, assisting their trafficking to lymph tissue.
3. Increasing cellular activity, such as proliferation and differentiation of immune cells and phagocytosis.

Figure: The Human Immune System. Image credit: Shutterstock

Other studies indicate that some pathogens, such as fungi, lose virulence at higher temperatures, further accounting for elevated body temperatures and the importance of the fever response. Of course, if body temperature becomes too high, it will compromise immune system function, moving it away from the temperature optimum and leading to other complications. So, the fever response must be carefully regulated.

Here’s the key point: the metabolic costs of endothermy are justified because warm-bloodedness allows the immune systems of birds and mammals to be near enough to the temperature optimum that infectious agents can be quickly cleared from their bodies.

Fever Response in Ectotherms

Cold-blooded animals (ectotherms) also mount a fever response to infectious agents for the same reason as endotherms. However, the body temperature of ectotherms is set by their surroundings. This limitation means that ectotherms need to regulate their body temperature and mount the fever response through their behavior by moving into spaces with elevated temperatures. Doing so places them at the mercy of environmental changes. This condition means that cold-blooded creatures experience a significant time lag between the onset of infection and the fever response. It also means that, in some cases, ectotherms can’t elevate their body temperature to the immune system optimum if, for example, it is night or overcast.

Finally, in an attempt to elevate their body temperatures, ectotherms need to be out from under cover, making themselves vulnerable to predators. So, according to Logan’s model, endothermy offers some tangible advantages compared to ectothermy.

But endothermy comes at a cost. As mentioned, the metabolic cost of endothermy is extensive compared to ectothermy. Pathogen virulence marks another disadvantage. Logan points out that pathogens that infect cold-blooded animals are much less virulent than pathogens that infect warm-blooded creatures.

Endothermy and Ectothermy Trade-Offs

So, when it comes to regulation of animal body temperature, a set of trade-offs exists that include:

• Metabolic costs
• Immune system responsiveness and effectiveness
• Pathogen virulence
• Vulnerability to predators

These trade-offs can be managed by two viable strategies: endothermy and ectothermy. Each has advantages and disadvantages. And each is optimized in its own right.

Regulation of Body Temperature and the Case for a Creator

Logan seeks to account for the evolutionary origins of endothermy by appealing to the advantages it offers organisms battling pathogens. But, examining Logan’s scenario leaves one feeling as if the explanation is little more than an evolutionary just-so story.

When endothermy presented an enigma for biologists, it would have been hard to argue that it reflected the handiwork of a Creator, particularly in light of its large metabolic cost. But now that scientists understand the trade-offs in play and the optimization associated with the endothermic lifestyle, we can also interpret the optimization of endothermy and ectothermy as evidence for design.

From my vantage point, optimization signifies the handiwork of a Creator. As I discuss in The Cell’s Design, saying something is optimized is equivalent to saying it is well-designed. The optimization of an engineered system doesn’t just happen. Rather, such systems require forethought, planning, and careful attention to detail. In the same way, the optimized designs of biological systems like endothermy and ectothermy reasonably point to the work of a Creator.

And I am chill with that.

Resources

• “The Fungus Is Not Among Us: Optimization of Mammalian Body Temperature” by Fazale Rana (article)
• “Q&A: Why Would a Limitless Creator Face Trade-Offs in Biochemical Designs” by Fazale Rana (article)

Sometimes I just can’t help myself. I know it’s clickbait but I click on the link anyway.

A few days ago, as a result of momentary weakness, I found myself reading an article from the ScoopWhoop website, “16 Things Most of Us Think Are the Same but Actually Aren’t.”

OK. OK. Now that you saw the title you want to click on the link, too.

To save you from wasting five minutes of your life, here is the ScoopWhoop list:

• Weather and Climate
• Turtle and Tortoise
• Jam and Jelly
• Eraser and Rubber
• Great Britain and the UK
• Pill and Tablet
• Shrimp and Prawn
• Butter and Margarine
• Orange and Tangerine
• Biscuits and Cookies
• Cupcakes and Muffins
• Mushrooms and Toadstools
• Tofu and Paneer
• Rabbits and Hares
• Alligators and Crocodiles
• Rats and Mice

And there you have it. Not a very impressive list, really.

If I were putting together a biochemist’s version of this list, I would start with synonymous mutations. Even though many life scientists think they are the same, studies indicate that they “actually aren’t.”

If you have no idea what I am talking about or what this insight has to do with the creation/evolution debate, let me explain by starting with some background information, beginning with the central dogma of molecular biology and the genetic code.

Central Dogma of Molecular Biology

According to this tenet of molecular biology, the information stored in DNA is functionally expressed through the activities of proteins. When it is time for the cell’s machinery to produce a particular protein, it copies the appropriate information from the DNA molecule through a process called transcription and produces a molecule called messenger RNA (mRNA). Once assembled, mRNA migrates to the ribosome, where it directs the synthesis of proteins through a process known as translation.

Figure 1: The central dogma of molecular biology. Image credit: Shutterstock

The Genetic Code

At first glance, there appears to be a mismatch between the stored information in DNA and the information expressed in proteins. A one-to-one relationship cannot exist between the four different nucleotides that make up DNA and the twenty different amino acids used to assemble proteins. The cell handles this mismatch by using a code comprised of groupings of three nucleotides, called codons, to specify the twenty different amino acids.

 

Figure 2: Codons. Image credit: Wikipedia

The cell uses a set of rules to relate these nucleotide triplet sequences to the twenty amino acids that comprise proteins. Molecular biologists refer to this set of rules as the genetic code. The nucleotide triplets represent the fundamental units of the genetic code. The code uses each combination of nucleotide triplets to signify an amino acid. This code is essentially universal among all living organisms.

Sixty-four codons make up the genetic code. Because the code only needs to encode twenty amino acids, some of the codons are redundant. That is, different codons code for the same amino acid. In fact, up to six different codons specify some amino acids. Others are specified by only one codon.¹

Figure 3: The genetic code. Image credit: Shutterstock

A little more background information about mutations will help fill out the picture.

Mutations

A mutation refers to any change that takes place in the DNA nucleotide sequence. DNA can experience several different types of mutations. Substitution mutations are one common type. When a substitution mutation occurs, one (or more) of the nucleotides in the DNA strand is replaced by another nucleotide. For example, an A may be replaced by a G, or a C may be replaced by a T. This substitution changes the codon. Interestingly, the genetic code is structured in such a way that when substitution mutations take place, the resulting codon often specifies the same amino acid (due to redundancy) or an amino acid that has similar chemical and physical properties to the amino acid originally encoded.

Synonymous and Nonsynonymous Mutations

When substitution mutations generate a new codon that specifies the same amino acid as initially encoded, it’s referred to as a synonymous mutation. However, when a substitution produces a codon that specifies a different amino acid, it’s called a nonsynonymous mutation.

Nonsynonymous mutations can be deleterious if they affect a critical amino acid or if they significantly alter the chemical and physical profile along the protein chain. If the substituted amino acid possesses dramatically different physicochemical properties from the native amino acid, it may cause the protein to fold improperly. Improper folding impacts the protein’s structure, yielding a biomolecule with reduced or even lost function.

On the other hand, biochemists have long thought that synonymous mutations have no effect on protein structure and function because these types of mutations don’t change the amino acid sequences of proteins. Even though biochemists think that synonymous mutations are silent—having no functional consequences—evolutionary biologists find ways to use them, including using patterns of synonymous mutations to establish evolutionary relationships.

Patterns of Synonymous Mutations and the Case for Biological Evolution

Evolutionary biologists consider shared genetic features found in organisms that naturally group together as compelling evidence for common descent. One feature of particular interest is the identical (or nearly identical) DNA sequence patterns found in genomes. According to this line of reasoning, the shared patterns arose as a result of a series of substitution mutations that occurred in the common ancestor’s genome. Presumably, as the varying evolutionary lineages diverged from the nexus point, they carried with them the altered sequences created by the primordial mutations.

Synonymous mutations play a significant role in this particular argument for common descent. Because synonymous mutations don’t alter the amino acid sequence of proteins, their effects are considered to be inconsequential. So, when the same (or nearly the same) patterns of synonymous mutations are observed in genomes of organisms that cluster together into the same group, most life scientists interpret them as compelling evidence of the organisms’ common evolutionary history.

It is conceivable that nonsynonymous mutations, which alter the protein amino acid sequences, may impart some type of benefit and, therefore, shared patterns of nonsynonymous changes could be understood as evidence for shared design. (See the last section of this article.) But this is not the case when it comes to synonymous mutations, which raises the question: Why would a Creator intentionally introduce new codons that code for the same amino acid into genes when these changes have no functional utility?

Apart from invoking a Creator, the shared patterns of synonymous mutations make perfect sense if genomes have been shaped by evolutionary processes and an evolutionary history. However, this argument for biological evolution (shared ancestry) and challenge to a creation model interpretation (shared design) hinges on the underlying assumption that synonymous mutations have no functional consequence.

But what if this assumption no longer holds?

Synonymous Mutations Are Not Interchangeable

Biochemists used to think that synonymous mutations had no impact whatsoever on protein structure and, hence, function, but this view is changing thanks to studies such as the one carried out by researchers at University of Colorado, Boulder.²

These researchers discovered synonymous mutations that increase the translational efficiency of a gene (found in the genome of Salmonella enterica). This gene codes for an enzyme that plays a role in the biosynthetic pathway for the amino acid arginine. (This enzyme also plays a role in the biosynthesis of proline.) They believe that these mutations alter the three-dimensional structure of the DNA sequence near the beginning of the coding portion of the gene. They also think that the synonymous mutations improve the stability of the messenger RNA molecule. Both effects would lead to greater translational efficiency at the ribosome.

As radical (and unexpected) as this finding may seem to be, it follows on the heels of other recent discoveries that also recognize the functional importance of synonymous mutations.³ Generally speaking, biochemists have discovered that synonymous mutations function to influence not only the rate and efficiency of translation (as the scientists from the University of Colorado, Bolder learned) and the folding of the proteins after they are produced at the ribosome.

Even though synonymous mutations leave the amino acid sequence of the protein unchanged, they can exert influence by altering the:

• regulatory regions of the gene that influence the transcription rate
• secondary and tertiary structure of messenger RNA that influences the rate of translation
• stability of messenger RNA that influences the amount of protein produced
• translation rate that influences the folding of the protein as it exits the ribosome

Biochemists are just beginning to come to terms with the significance of these discoveries, but it is already clear that synonymous mutations have biomedical consequences.⁴ They also impact models for molecular evolution. But for now, I want to focus on the impact these discoveries has on the creation/evolution debate.

Patterns of Synonymous Mutations and the Case for Creation

As noted, many people consider the most compelling evidence for common descent to be the shared genetic features displayed by organisms that naturally cluster together. But if life is the product of a Creator’s handiwork, the shared genetic features could be understood as shared designs deployed by a Creator. In fact, a historical precedent exists for the common design interpretation. Prior to Darwin, biologists viewed shared biological features as manifestations of archetypical designs that existed in the Creator’s mind.

But the common design interpretation requires that the shared features be functional. (Or, that they arise independently in a nonrandom manner.) For those who view life from the framework of the evolutionary paradigm, the shared patterns of synonymous mutations invalidate the common design explanation—because these mutations are considered to be functionally insignificant.

But in the face of mounting evidence for the functional importance of synonymous mutations, this objection to common design has begun to erode. Though many life scientists are quick to dismiss the common design interpretation of biology, advances in molecular biology continue to strengthen this explanation and, with it, the case for a Creator.

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)
• “Biochemical Synonyms Optimized, Part 1” by Fazale Rana (article)
• “Biochemical Synonyms Optimized, Part 2” by Fazale Rana (article)
• “Nonrandom Mutations Scramble the Case for Common Descent” by Fazale Rana (article)
• “Alu Sequences in Primate Genomes: Evidence for Common Descent or Common Design?” by Fazale Rana (article)
• “Archetype or Ancestor? Sir Richard Owen and the Case for Design” by Fazale Rana (article)