Origins of Monogamy Cause Evolutionary Paradigm Breakup

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BY FAZALE RANA – MARCH 20, 2019

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.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

Endnotes
  1. Mark Binelli, “Gregg Allman: The Lost Brother,” Rolling Stone, no. 1082/1083 (July 9–23, 2009), https://www.rollingstone.com/music/music-features/gregg-allman-the-lost-brother-108623/.
  2. Binelli, “Gregg Allman: The Lost Brother.”
  3. Rebecca L. Young et al., “Conserved Transcriptomic Profiles underpin Monogamy across Vertebrates,” Proceedings of the National Academy of Sciences, USA 116, no. 4 (January 22, 2019): 1331–36, doi:10.1073/pnas.1813775116.
  4. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W. W. Norton & Company, 1990).
  5. Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (New York: Cambridge University Press, 2003); George McGhee, Convergent Evolution: Limited Forms Most Beautiful (Cambridge, MA: MIT Press, 2011).
  6. University of Texas at Austin, “Evolution Used Same Genetic Formula to Turn Animals Monogamous,” ScienceDaily (January 7, 2019), www.sciencedaily.com/releases/2019/01/1901071507.htm.

Reprinted with permission by the author
Original article at:
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Believing Impossible Things: Convergent Origins of Functional Junk DNA Sequences

believingimpossiblethings

BY FAZALE RANA – MARCH 14, 2018

In a classic scene from Alice in Wonderland, the story’s heroine informs the White Queen, “One can’t believe impossible things,” to which, the White Queen—scolding Alice—replies, “I daresay you haven’t had much practice. When I was your age, I always did it for half-an-hour a day. Why, sometimes I’ve believed as many as six impossible things before breakfast.”

If recent work by researchers from UC Santa Cruz and the University of Rochester (New York) is to be taken as true, it would require evolutionary biologists to believe two impossible things—before, during, and after breakfast. These scientific investigators have discovered something that is hard to believe about the role SINE DNA plays in gene regulation, raising questions about the validity of the evolutionary explanation for the architecture of the human genome.1 In fact, considering the implications of this work, it would be easier to believe that the human genome was shaped by a Creator’s handiwork than by evolutionary forces.

SINE DNA

One of the many classes of noncoding or junk DNA, short interspersed elements, or SINE DNA sequences, range in size from 100 to 300 base pairs (genetic letters). In primates, the most common SINEs are the Alu sequences. There are about 1.1 million Alu copies in the human genome (roughly 12 percent of the genome).

SINE DNA sequences (including Alu sequences) contain a DNA segment used by the cell’s machinery to produce an RNA message. This feature allows SINEs to be transcribed. Because of this feature, molecular biologists also categorize SINE DNA as a retroposon. Molecular biologists believe that SINE sequences can multiply in number within an organism’s genome through the activity of the enzyme, reverse transcriptase. Presumably, once SINE DNA becomes transcribed, reverse transcriptase converts SINE RNA back into DNA. The reconverted DNA sequence then randomly reintegrates back into the genome. It’s through this duplication and reintegration mechanism that SINE sequences proliferate as they move around, or retrotranspose, throughout the genome. To say it differently, molecular biologists believe that over time, transcription of SINE DNA and reverse transcription of SINE RNA increases the copy number of SINE sequences and randomly disperses them throughout an organism’s genome.

Molecular biologists have discovered numerous instances in which nearly identical SINE segments occur at corresponding locations in the genomes of humans, chimpanzees, and other primates. Because the duplication and movement of SINE DNA appear to be random, evolutionary biologists think it unlikely that SINE sequences would independently appear in the same locations in the genomes of humans and chimpanzees (and other primates). And given their supposed nonfunctional nature, shared SINE DNA in humans and chimpanzees seemingly reflects their common evolutionary ancestry. In fact, evolutionary biologists have gone one step further, using SINE Alu sequences to construct primate evolutionary trees.

SINE DNA Is Functional

Even though many people view shared junk DNA sequences as the most compelling evidence for biological evolution, the growing recognition that virtually every class of junk DNA has function undermines this conclusion. For if these shared sequences are functional, then one could argue that they reflect the Creator’s common design, not shared evolutionary ancestry and common descent. As a case in point, in recent years, molecular biologists have learned that SINE DNA plays a vital role in gene regulation through a variety of distinct mechanisms.2

Staufen-Mediated mRNA Decay

One way SINE sequences regulate gene expression is through a pathway called Staufen-mediated messenger RNA (mRNA) decay (SMD). Critical to an organism’s development, SMD plays a key role in cellular differentiation. SMD is characterized by a complex mechanism centered around the destruction of mRNA. When this degradation takes place, it down-regulates gene expression. The SMD pathway involves binding of a protein called Staufen-1 to one of the ends of the mRNA molecule (dubbed the 3´untranslated region). Staufen-1 binds specifically to double-stranded structures in the 3´untranslated region. This double strand structure forms when Alu sequences in the 3´untranslated region bind to long noncoding RNA molecules containing Alu sequences. This binding event triggers a cascade of additional events that leads to the breakdown of messenger RNA.

Common Descent or Common Design?

As an old-earth creationist, I see the functional role played by noncoding DNA sequences as a reflection of God’s handiwork, defending the case for design from a significant evolutionary challenge. To state it differently: these findings mean that it is just as reasonable to conclude that the shared SINE sequences in the genomes of humans and the great apes reflect common design, not a shared evolutionary ancestry.

In fact, I would maintain that it is more reasonable to think that functional SINE DNA sequences reflect common design, rather than common descent, given the pervasive role these sequence elements play in gene regulation. Because Alu sequences are only found in primates, they must have originated fairly recently (when viewed from an evolutionary framework). Yet, they play an integral and far-reaching role in gene regulation.

And herein lies the first impossible thing evolutionary biologists must believe: Somehow Alusequences arose and then quickly assumed a central place in gene regulation. According to Carl Schmid, a researcher who uncovered some of the first evidence for the functional role played by SINE DNA, “Sine Alus have appeared only recently within the primate lineage, this proposal [of SINE DNA function] provokes the challenging question of how Alu RNA could have possibly assumed a significant role in cell physiology.”3

How Does Junk DNA Acquire Function?

Still, those who subscribe to the evolutionary framework do not view functional junk DNA as incompatible with common descent. They argue that junk DNA acquired function through a process called neofunctionalization. In the case of SMD mediated by Alu sequences in the human genome, evolutionary biologists maintain that occasionally these DNA elements will become incorporated into the 3´untranslated regions of genes and regions of the human genome that produce long noncoding RNAs, and, occasionally, by chance, some of the Alusequences in long noncoding RNAs will have the capacity to pair with the 3´untranslated region of specific mRNAs. When this happens, these Alu sequences trigger SMD-mediated gene regulation. And if this gene regulation has any advantage, it will persist so that over time, some Alu sequences will eventually evolve to assume a role in SMD-mediated gene regulation.

Is Neofunctionalization the Best Explanation for SINE Function?

At some level, this evolutionary scenario seems reasonable (the concerns expressed by Carl Schmid notwithstanding). Still, neofunctionalization events should be relatively rare. And because of the chance nature of neofunctionalization, it would be rational to think that the central role SINE sequences play in SMD gene regulation would be unique to humans.

Why would I make this claim? Based on the nature of evolutionary mechanisms, chance should govern biological and biochemical evolution at its most fundamental level (assuming it occurs). Evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection, which also 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. According to Gould,

“No finale can be specified at the start, none would ever occur a second time in the same way, because any pathway proceeds through thousands of improbable stages. Alter any early event, ever so slightly, and without apparent importance at the time, and evolution cascades into a radically different channel.”4

To help clarify the concept of historical contingency, Gould used the metaphor of “replaying life’s tape.” If one were to push the rewind button, erase life’s history, and let the tape run again, the results would be completely different each time. The very essence of the evolutionary process renders evolutionary outcomes nonrepeatable.

Gould’s perspective of the evolutionary process has been affirmed by other researchers who have produced data, indicating that if evolutionary processes explain the origin of biochemical systems, they must be historically contingent.

Did SMD Evolve Twice?

Yet, collaborators from UC Santa Cruz and the University of Rochester discovered that SINE-mediated SMD appears to have evolved independently—two separate times—in humans and mice, the second impossible thing evolutionary biologists have to believe.

Though rodents don’t possess Alu sequences, they do possess several other SINE elements, labeled B1, B2, B4, and ID. Remarkably, these B/ID sequences occur in regions of the mouse genome corresponding to regions of the human-harboring Alu sequences. And, when the B/ID sequences are associated with the 3´untranslated regions of genes, the mRNA produced from these genes is down-regulated, suggesting that these genes are under the influence of the SMD-mediated pathway—an unexpected result.

But, this finding is not nearly as astonishing as something else the research team discovered. By comparing about 1,200 human-mouse gene pairs in myoblasts, the researchers discovered 24 genes in this cell type that were identical in the human and mouse genomes. These identical genes performed the same physiological role and possessed SINE elements (Alu and B/ID, respectively) and were regulated by the SMD mechanism.

Evolutionary biologists believe that Alu and B/ID SINE sequences emerged independently in the rodent and human lineages. If so, this means that the evolutionary processes must have independently produced the identical outcome—SINE-mediated SMD gene regulation—24 separate times for each of the 24 identical genes. As the researchers point out, chance alone cannot explain their findings. Yet, evolutionary mechanisms are historically contingent and should not yield identical outcomes. This impossible scenario causes me to question if neofunctionalization is the explanation for functional SINE DNA.

And yet, this is not the first time that life scientists have discovered the independent emergence of identical function for junk DNA sequences.

So, which is the better explanation for functional junk DNA sequences: neofunctionalization through historically contingent evolutionary processes or the work of a Mind?

As Alice emphatically complained, “One can’t believe impossible things.”

Resources

Endnotes

  1. Brownyn A. Lucas et al., “Evidence for Convergent Evolution of SINE-Directed Staufen-Mediated mRNA Decay,” Proceedings of the National Academy of Sciences, USA Early Edition (January 2018): doi:10.1073/pnas.1715531115.
  2. Reyad A. Elbarbary et al., “Retrotransposons as Regulators of Gene Function,” Science 351 (February 12, 2016): doi:10.1126/science.aac7247.
  3. Carl W. Schmid, “Does SINE Evolution Preclude Alu Function?” Nucleic Acid Research 26 (October 1998): 4541–50, doi:10.1093/nar/26.20.4541.
  4. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W. W. Norton & Company, 1989), 51.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2018/03/14/believing-impossible-things-convergent-origins-of-functional-junk-dna-sequences

Like a Fish Out of Water: Why I’m Skeptical of the Evolutionary Paradigm

likeafishoutofwater

BY FAZALE RANA – JULY 27, 2016

I am skeptical that evolutionary processes can fully account for life’s origin, history, and design—and that often makes me feel like a fish out of water.

“Mainstream” scientists view biological evolution as the organizing principle in biology. In fact, Russian geneticist Theodosius Dobzhansky famously wrote, “Nothing in biology makes sense except in the light of evolution.”1 So, when I question evolutionary explanations, I become an outsider. I am outside the fish bowl, looking in. Because I’m a biochemist, my critics accuse me of being either dishonest or incompetent. Why else would I question the “fact” of evolution in the face of the overwhelming evidence for common descent? They claim that theological—not scientific motivations fuel my skepticism.

I would partially agree with that assessment. I find it hard to square certain features of the evolutionary framework with some of Christianity’s most important biblical and theological ideas. But, I also think that there are some very real scientific problems associated with the evolutionary paradigm. The deficiencies are best exposed by failed predictions.

From my perspective, the unpredicted pervasiveness of convergence justifies skepticism about evolution’s capacity to fully account for the history and diversity of life on Earth. Convergence stands as a failed prediction.

Convergence

One of evolution’s failed predictions relates to the phenomenon known as convergence. This concept describes instances in which unrelated organisms possess nearly identical anatomical and physiological characteristics. Presumably, evolutionary pathways independently produced these identical (or near identical) features. Yet convergence doesn’t make much sense from an evolutionary perspective. Indeed, if evolution is responsible for the diversity of life, one would expect convergence to be extremely rare. As a I wrote in a previous blog post, the mechanism that drives the evolutionary process consists of an extended sequence of unpredictable, chance events. Given this mechanism, it seems improbable that disparate evolutionary pathways would ever lead to the same biological feature. To put it another way, examples of convergence should be rare.

The concept of historical contingency embodies the notion that evolution should be nonrepeatable, and is the theme of Stephen Jay Gould’s book Wonderful Life.2 To help clarify the concept of historical contingency, 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.

Yet, biological convergence is widespread.3 Recently, researchers from the University of New South Wales (in Australia) added to the examples of convergence at an organismal level. From an evolutionary perspective, they showed that amphibious behavior in fish evolved 33 separate times among extant groups! In fact, in one family, fish adopted a terrestrial life style between 3 to 7 times.

This result was unexpected. One of the researchers involved with the study stated, “Because of the challenges fish face in being able to breathe and move and reproduce on land, it had been thought this was a rare occurrence.”4

Recently, another team of investigators from the University of Kansas identified another example of biochemical convergence. They showed that venom evolved, separately and independently, 18 times in fish that live in freshwater and marine environments. This result is all the more surprising because—as William Leo Smith, one of the study’s authors points out— “fish venoms are often super complicated, big molecules.”5

Does the Widespread Occurrence of Convergence Falsify Evolution?

From my perspective, the unpredicted pervasiveness of convergence justifies skepticism about evolution’s capacity to fully account for the history and diversity of life on Earth. It stands as a failed prediction. Yet many evolutionary biologists don’t see it that way. For example, the scientists from the University of New South Wales responded to their unexpected find this way: “Now we have shown this initial transition to land is quite common, it seems these challenges can be readily overcome.”6 However, their interpretation entails circular reasoning. Biologists thought that fish moving to land would be difficult given the immense challenges associated with this transition. But, when it was found to be a frequent occurrence, then they conclude it must be easy. But they have no reason to think it must be easy other than the widespread occurrence of this transition. I would contend that this circular reasoning reflects a deep-seated, a priori commitment to the evolutionary paradigm, in which evolution is accepted as fact, and no evidence can ever count against it.

Convergence and the Case for Intelligent Design

Though the idea of convergence fits awkwardly within the evolutionary framework, it makes perfect sense if a Creator is responsible for life. Instead of convergent features emerging through repeated evolutionary outcomes, they could be understood as reflecting the work 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.

Resources
The Cell’s Design (book)

Endnotes
  1. Theodosius Dobzhansky, “Nothing in Biology Makes Sense Except in the Light of Evolution,” American Biology Teacher 35 (March 1971): 125–29.
  2. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W.W. Norton & Company, 1990).
  3. Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (New York: Cambridge University Press, 2003); George McGhee, Convergent Evolution: Limited Forms Most Beautiful (Cambridge, MA: MIT Press, 2011).
  4. University of New South Wales, “Fish Out of Water Are More Common Than Thought,” ScienceDaily, June 22, 2016, https://www.sciencedaily.com/releases/2016/06/160622102129.htm.
  5. University of Kansas, “Researchers Tally Huge Number of Venomous Fishes, Tout Potential for Medical Therapies,” ScienceDaily, July 5, 2016, https://www.sciencedaily.com/releases/2016/07/160705160206.htm.
  6. “Fish Out of Water,” ScienceDaily.
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Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2016/07/27/like-a-fish-out-of-water-why-i’m-skeptical-of-the-evolutionary-paradigm

Historical Contingency and the Improbability of Protein Evolution, Part 2 (of 2)

historicalcontingencyandtheimprobability

BY FAZALE RANA – JULY 20, 2016

A few weeks ago, Kathy Emmons of WORD FM in Pittsburg interviewed me about the connection between human evolution and human trafficking. During the interview, she asked me if theological or scientific concerns drove my skepticism about human evolution. My answer is both.

I find it difficult to reconcile the idea of human evolution with passages in the Old and New Testaments that address human origins. But, I also think that there are significant scientific problems confronting the evolutionary paradigm. A recent study by scientists from the Universities of Oregon and Chicago highlights one of those scientific challenges.1

As described in a previous post, these researchers wanted to develop a better understanding of the role that chance historical events play in evolutionary processes. To do this, they reconstructed what they believe to be the evolutionary pathway that led to the emergence of the cortisol-specific glucocorticoid receptor protein, a key component of the vertebrate endocrine system. Based on their reconstruction, it appears that seven amino acid changes transformed the ancestral receptor protein into one that exclusively binds cortisol. They determined that two of the changes were permissive. That is, these changes do not contribute to the binding specificity of the glucocorticoid receptor, but must occur before any of the functional changes took place. Based on their analysis, it appears that the permissive changes were highly improbable, leading the researchers to conclude that historical contingency plays a central role in evolutionary transformations.

According to the researchers:

“If evolutionary history could be replayed from the ancestral starting point, the same kind of permissive substitutions would be unlikely to occur. The transition to GR’s [glucocorticoid receptor’s] present form and function would likely be inaccessible, and different outcomes would almost certainly ensue. Cortisol-specific signaling might evolve by a different mechanism in the GR . . . or the vertebrate endocrine system more generally—would be substantially different.”2

Historical Contingency

The concept of historical contingency is the theme of the late Stephen Jay Gould’s book Wonderful Life.3 According to this idea, the evolutionary process consists of an extended sequence of unpredictable, chance events. 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.

Gould envisioned historical contingency as primarily resulting from external events (such as climate change or asteroid impacts). But this latest work indicates that the intrinsic complexity of proteins also contributes to historical contingency, because of the necessity and low probability of of permissive amino acid substitutions that support functional changes.

How Widespread Is Historical Contingency?

The question then becomes: How widely applicable is this result? The research team from the Universities of Oregon and Chicago expressed uncertainty regarding this point, but other studies indicate that historical contingency must play a prominent role in molecular evolution.

For example, the long-term evolution experiment conducted by Richard Lenski’s group at Michigan State University demonstrated that the emergence of citrate metabolism in E. coliunder aerobic conditions was historically contingent, predicated on a sequence of chance molecular events. (For more information, see the articles listed under “Resources.”)

Using simulations to monitor the evolution of a protein dubbed argT, researchers from the University of Pennsylvania showed that genetic mutations selected by the evolutionary process are dependent on previous mutations, and over time it becomes increasingly difficult to reverse mutational transformations.4 In other words, an amino acid substitution that occurs in a protein today and is accepted by the evolutionary process would most likely be deleterious if it occurred in the past (because of the central role permissive substitutions play in evolutionary history). Consequently, this mutational change would be selected against by the evolutionary process. One of the researchers involved in this study, Joshua Plotkin, stated,

“There is intrinsically a huge amount of contingency in evolution. Whatever mutations happen to come first set the stage for what other later mutations are permissible. Indeed, history channels evolution down a certain path. Gould’s famous tape of life would be very different if replayed, even more different than Gould might have imagined.”5

A Failed Prediction of the Evolutionary Paradigm

Because the evolutionary process is historically contingent, it seems unlikely that evolutionary processes would lead to identical or nearly identical outcomes. Yet, when viewed from an evolutionary standpoint, it appears as if repeated evolutionary outcomes have been 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.6 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.

I regard the widespread occurrence of convergence to one of evolution’s failed predictions, and, as I told Kathy Emmons, a justifiable reason to be skeptical of the claim that evolutionary processes can fully explain the history, diversity, and design of life.

In an upcoming blog post, I will further explore the challenge convergence poses for the evolutionary paradigm.

Stay tuned… (or set your tape player to “record.”)

 

Resources

Endnotes

  1. Michael Harms and Joseph Thornton, “Historical Contingency and Its Biophysical Basis in Glucocorticoid Receptor Evolution,” Nature 512 (August 2014): 203–07, doi:10.1038/nature13410.
  2. Ibid., 207.
  3. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W.W. Norton & Company, 1990).
  4. Premal Shah, David McCandlish, and Joshua Plotkin, “Contingency and Entrenchment in Protein Evolution under Purifying Selection,” Proceedings of the National Academy of Sciences, USA 112 (June 2015): E3226–E3235, doi: 10.1073/pnas.1412933112.
  5. University of Pennsylvania, “Evolution Is Unpredictable and Irreversible, Biologists Show,” ScienceDaily,June 8, 2015, sciencedaily.com/releases/2015/06/150608213032.htm.
  6. Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (New York: Cambridge University Press, 2003); George McGhee, Convergent Evolution: Limited Forms Most Beautiful (Cambridge, MA: MIT Press, 2011).
Reprinted with permission by the author
Original article at:
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