ATP Transport Challenges the Evolutionary Origin of Mitochondria


By Fazale Rana – August 21, 2019

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


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

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

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

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

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

The Endosymbiont Hypothesis

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

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

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


Image: Endosymbiont Hypothesis. Image credit: Wikipedia

Evidence for the Endosymbiont Hypothesis

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

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

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

The Role of Mitochondria

Mitochondria serve cells in a number of ways, including:

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

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

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


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

ATP Production and Transport

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

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

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

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

The Problem ATP Transport Causes for The Endosymbiont Hypothesis

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

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

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

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

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

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

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

Two Alternative Models

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

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

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

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

Moving Forward, Or Moving Backward?

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

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

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

According to the authors, this means that:

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

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

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

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

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

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

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


Challenges to the Endosymbiont Hypothesis:

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

ATP Production and the Case for a Creator:

  1. Zhang Wang and Martin Wu, “Phylogenomic Reconstruction Indicates Mitochondrial Ancestor Was an Energy Parasite,” PLOS One 9, no. 10 (October 15, 2014): e110685, doi:10.1371/journal.pone.0110685.
  2. Franklin M. Harold, In Search of Cell History: The Evolution of Life’s Building Blocks (Chicago, IL: The University of Chicago Press, 2014), 131.
  3. Harold, In Search of Cell History, 131.
  4. Harold, In Search of Cell History, 132.
  5. Wang and Wu, “Phylogenomic Reconstruction.”
  6. Wang and Wu, “Phylogenomic Reconstruction.”

Reprinted with permission by the author

Original article at:

Evolutionary Paradigm Lacks Explanation for Origin of Mitochondria and Eukaryotic Cells



You carried the cross
Of my shame
Oh my shame
You know I believe it
But I still haven’t found
What I’m looking for

—Adam Clayton, Dave Evans, Larry Mullen, Paul David Hewson, Victor Reina

One of my favorite U2 songs is “I Still Haven’t Found What I’m Looking For.” For me, it’s a reminder that because of Christ, my life has meaning, purpose, and a sense of destiny. Still, I will never discover ultimate fulfillment in this world no matter how hard I search, but in the world to come—the new heaven and new earth.

Though their pursuit is scientific and not religious, many scientists have also failed to find what they have been looking for. Physicists are on a quest to find the Theory of Everything—a Grand Unified Theory (GUT) that can account for everything in physics. However, a GUT eludes them.

On the other hand, life scientists appear to have found it. They claim to have discovered biology’s GUT: the theory of evolution. Many biologists assert that evolutionary mechanisms can fully account for the origin, history, and design of life. And they are happy to sing about their discovery any chance they get.

Yet, despite this claim, the evolutionary paradigm seems to come up short time and time again when it comes to explaining key events in life’s history. And this failure serves as the basis for my skepticism regarding the evolutionary paradigm.

Currently, evolutionary biologists lack explanations for the key transitions in life’s history, including thes

  • origin of life,
  • origin of eukaryotic cells,
  • origin of sexual reproduction,
  • origin of body plans,
  • origin of consciousness,
  • and the origin of human exceptionalism.

To be certain, evolutionary biologists have proposed models to explain each of these transitions, but the models consistently fail to deliver, as a recent review article published by two prominent evolutionary biologists from the Hungarian Academy of Sciences illustrates.In this article, these researchers point out the insufficiency of the endosymbiont hypothesis—the leading evolutionary model for the origin of eukaryotic cells—to account for the origin of mitochondria and, hence, eukaryogenesis.

The Endosymbiont Hypothesis

Lynn Margulis (1938–2011) advanced the endosymbiont hypothesis for the origin of eukaryotic cells in the 1960s, building on the ideas of Russian botanist, Konstantin Mereschkowski. Taught in introductory high school and college biology courses, Margulis’s work has become a cornerstone idea of the evolutionary paradigm. This classroom exposure explains why students often ask me about the endosymbiont hypothesis when I speak on university campuses. Many first-year biology students and professional life scientists alike find the evidence for this idea compelling and, consequently, view it as providing broad support for an evolutionary explanation for the history and design of life.

According to the hypothesis, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe. (Ingested cells that take up permanent residence within other cells are referred to as endosymbionts.)

Presumably, organelles such as mitochondria were once endosymbionts. Once engulfed, the endosymbionts took up permanent residency within the host, with the endosymbiont growing and dividing inside the host. Over time, the endosymbionts and the host became mutually interdependent, with the endosymbionts providing a metabolic benefit for the host cell. The endosymbionts gradually evolved into organelles through a process referred to as genome reduction. This reduction resulted when genes from the endosymbionts’ genomes were transferred into the genome of the host organism. Eventually, the host cell evolved the machinery to produce the proteins needed by the former endosymbiont and processes to transport those proteins into the organelle’s interior.

Evidence for the Endosymbiont Hypothesis

The similarity between organelles and bacteria serve as the main line of evidence for the endosymbiont hypothesis. For example, mitochondria—which are believed to be descended from a group of alpha-proteobacteria—are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

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

The presence of the unique lipid, cardiolipin, in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. This important lipid component of bacterial inner membranes is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider it a signature lipid for mitochondria and a vestige of this organelle’s evolutionary history.2

Does the Endosymbiont Hypothesis Successfully Account for the Origin of Mitochondria?

Despite the seemingly compelling evidence for the endosymbiont hypothesis, evolutionary biologists lack a genuine explanation for the origin of mitochondria, and, in a broader context, the origin of eukaryotic cells. In their recently published critical review, Zachar and Szathmary point out that evolutionary biologists have proposed over twenty different evolutionary scenarios for the mitochondrial origins that umbrella underneath the endosymbiont hypothesis. Of these, they identify eight that are reasonable, casting the others aside. Still, these eight hypotheses fail to fully account for the origin of mitochondria. The Hungarian biologists delineate twelve questions that any successful endosymbiogenesis model must answer. In turn, they demonstrate that none of these models answers all the questions. In doing so, the two researchers call for a new theory.

In the article’s abstract, the authors state, “The origin of mitochondria is a unique and hard evolutionary problem, embedded within the origin of eukaryotes. . . . Contending theories widely disagree on ancestral partners, initial conditions and unfolding events. There are many open questions but there is no comparative examination of hypotheses. We have specified twelve questions about the observable facts and hidden processes leading to the establishment of the endosymbiont that a valid hypothesis must address. There is no single theory capable of answering all questions.”3

Space doesn’t permit me to discuss each of the questions posed by the pair of biologists. Still, I would like to call attention to a few problems confronting the endosymbiont hypothesis, highlighted in their critical review.

Lack of Transitional Intermediates. Biologists have yet to discover any single-celled organisms that represent transitional intermediates between prokaryotes and eukaryotic cells. (There are some eukaryotes that lack mitochondria, but they appear to have lost these organelles.) All complex cells display the eukaryotic hallmark features. In other words, it looks as if eukaryotic cells emerged in a short period of time, without any transitional forms. In fact, some biologists dub the transition the eukaryotic big bang.

Chimeric Nature of Eukaryotic Cells. Eukaryotic cells possess an unusual combination of features. Their information-processing systems resemble those of archaea, but their membranes and energy metabolism are bacteria-like. There is no plausible evolutionary scenario to explain this blend of features. It would require the archaeon host to replace its membranes while retaining all its information-processing genes. Evolutionary biologists know of no instance in which this type of transition took place, nor do they know how it could have occurred.

Absence of Membrane Bioenergetics in the Host. All prokaryotic organisms rely on their plasma membrane to produce energy. If eukaryotic cells emerged via endosymbiogenesis, then the plasma membranes of eukaryotic cells should possess vestiges of that past function. Yet, the plasma membranes of eukaryotic cells show no traces of this essential biochemical feature.

Mechanism of Inclusion. The most plausible way for the endosymbiont to be taken up by the host cell is through a process called phagocytosis. But why wouldn’t the engulfed cell be digested by the host? How did the endosymbiont escape destruction? And, if it somehow survived, why doesn’t the mitochondria possess a triple membrane system, with the outermost membrane derived from the phagosome?

Early Selective Advantage. Once inside the host, why didn’t the endosymbiont simply reproduce, overrunning the host cell? What benefit would it be for the host cell to initially harbor the endosymbiont? Currently, evolutionary biologists don’t have answers to troubling questions such as these.

The challenges delineated by the Hungarian biologists aren’t the only ones faced by evolutionary models for endosymbiogenesis. As I discuss in a previous article, mitochondrial protein biogenesis poses another difficult problem for the endosymbiont hypothesis.

The authors of the critical review sum it up this way: “The integration of mitochondria was a major transition, and a hard one. It poses puzzles so complicated that new theories are still generated 100 years since endosymbiogenesis was first proposed by Konstantin Mereschkowsky and 50 years since Lynn Margulis cemented the endosymbiotic origin of mitochondria into evolutionary biology. . . . One would expect that by this time, there is a consensus about the transition, but far from that even the most fundamental points are still debated.”4

Though evolutionary biologists claim to have life’s history all figured out, in reality they are like most of us—they still haven’t found what they are looking for.



  1. Istvan Zachar and Eors Szathmary, “Breath-Giving Cooperation: Critical Review of Origin of Mitochondria Hypotheses,” Biology Direct 12 (August 14, 2017): 19, doi:10.1186/s13062-017-0190-5.
  2. In previous posts (herehere, and here), I explain the rationale for mitochondrial DNA and the presence of cardiolipin in the inner mitochondrial membrane from a creation model/intelligent design vantage point and, in doing so, demonstrate that the two biochemical features aren’t uniquely explained by the endosymbiont hypothesis.
  3. Zachar and Szathmary, “Breath-Giving Cooperation.”
  4. Zachar and Szathmary, “Breath-Giving Cooperation.”
Reprinted with permission by the author
Original article at:

Dollo’s Law at Home with a Creation Model, Reprised*



*This article is an expanded and updated version of an article published in 2011 on

Published posthumously, Thomas Wolfe’s 1940 novel, You Can’t Go Home Againconsidered by many to be his most significant work—explores how brutally unfair the passage of time can be. In the finale, George Webber (the story’s protagonist) concedes, “You can’t go back home” to family, childhood, familiar places, dreams, and old ways of life.

In other words, there’s an irreversible quality to life. Call it the arrow of time.

Like Wolfe, most evolutionary biologists believe there is an irreversibility to life’s history and the evolutionary process. In fact, this idea is codified in Dollo’s Law, which states that an organism cannot return, even partially, to a previous evolutionary stage occupied by one of its ancestors. Yet, several recent studies have uncovered what appears to be violations of Dollo’s Law. These violations call into question the sufficiency of the evolutionary paradigm to fully account for life’s history. On the other hand, the return to ‘ancestral states’ finds an explanation in an intelligent design/creation model approach to life’s history.

Dollo’s Law

French paleontologist Louis Dollo formulated the law that bears his name in 1893 before the advent of modern-day genetics, basing it on patterns he unearthed from the fossil record. Today, his idea finds undergirding in contemporary understanding of genetics and developmental biology.

Evolutionary biologist Richard Dawkins explains the modern-day conception of Dollo’s Law this way:

“Dollo’s Law is really just a statement about the statistical improbability of following exactly the same evolutionary trajectory twice . . . in either direction. A single mutational step can easily be reversed. But for larger numbers of mutational steps . . . mathematical space of all possible trajectories is so vast that the chance of two trajectories ever arriving at the same point becomes vanishingly small.”1

If a biological trait is lost during the evolutionary process, then the genes and developmental pathways responsible for that feature will eventually degrade, because they are no longer under selective pressure. In 1994, using mathematical modeling, researchers from Indiana University determined that once a biological trait is lost, the corresponding genes can be “reactivated” with reasonable probability over time scales of five hundred thousand to six million years. But once a time span of ten million years has transpired, unexpressed genes and dormant developmental pathways become permanently lost.2

In 2000, a scientific team from the University of Oregon offered a complementary perspective on the timescale for evolutionary reversals when they calculated how long it takes for a duplicated gene to lose function.3 (Duplicated genes serve as a proxy for dormant genes rendered useless because the trait they encode has been lost.) According to the evolutionary paradigm, once a gene becomes duplicated, it is no longer under the influence of natural selection. That is, it undergoes neutral evolution, and eventually becomes silenced as mutations accrue. As it turns out, the half-life for this process is approximately four million years. To put it another way, sixteen to twenty-four million years after the duplication event, the duplicated gene will have completely lost its function. Presumably, this result applies to dormant, unexpressed genes rendered unnecessary because the trait they specify is lost.

Both scenarios assume neutral evolution and the accumulation of mutations in a clockwise manner. But what if the loss of gene function is advantageous? Collaborative work by researchers from Harvard University and NYU in 2007 demonstrated that loss of gene function can take place on the order of about one million years if natural selection influences gene loss.4 This research team studied the loss of eyes in the cave fish, the Mexican tetra. Because they live in a dark cave environment, eyes serve no benefit for these creatures. The team discovered that eye reduction offers an advantage for these fish, because of the high metabolic cost associated with maintaining eyes. The reduced metabolic cost associated with eye loss accelerates the loss of gene function through the operation of natural selection.

Based on these three studies, it is reasonable to conclude that once a trait has been lost, the time limit for evolutionary reversals is on the order of about 20 million years.

The very nature of evolutionary mechanisms and the constraints of genetic mutations make it extremely improbable that evolutionary processes would allow an organism to revert to an ancestral state or to recover a lost biological trait. You can’t go home again.

Violations of Dollo’s Law

Despite this expectation, over the course of the last several years, researchers have uncovered several instances in which Dollo’s Law has been violated. A brief description of a handful of these occurrences follows:

The re-evolution of mandibular teeth in the frog genus Gastrotheca. This group is the only one that includes living frogs with true teeth on the lower jaw. When examined from an evolutionary framework, mandibular teeth were present in ancient frogs and then lost in the ancestor of all living frogs. It also looks as if teeth have been absent in frogs for 225 million years before they reappeared in Gastrotheca.5

The re-evolution of oviparity in sand boas. When viewed from an evolutionary perspective, it appears as if live-birth (viviparity) evolved from egg-laying (oviparity) behaviors in reptiles several times. For example, estimates indicate that this evolutionary transition has occurred in snakes at least thirty times. As a case in point, there are 41 species of boas in the Old and New Worlds that give live births. Yet, two recently described sand boas, the Arabian sand boas (Eryx jayakari) and the Saharan sand boa (Eryx muelleri) lay eggs. Phylogenetic analysis carried out by researchers from Yale University indicates that the egg-laying in these two species of sand boas re-evolved 60 million years after the transition to viviparity took place.6

The re-evolution of rotating sex combs in Drosophila. Sex combs are modified bristles unique to male fruit flies, used for courtship and mating. Compared to transverse sex combs, rotating sex combs result when several rows of bristles undergo a rotation of ninety degrees. In the ananassae fruit fly group most of the twenty or so species have simple transverse sex combs, with Drosophila bipectinata and Drosophila parabipectinata the two exceptions. These fruit fly species possess rotating sex combs. Phylogenetic analysis conducted by investigators from the University of California, Davis indicates that the rotating sex combs in these two species re-evolved, twelve million years after being lost.7

The re-evolution of sexuality in mites belonging to the taxa, Crotoniidae. Mites exhibit a wide range of reproductive modes, including parthenogenesis. In fact, this means of reproduction is prominent in the group Oribatida, clustering into two subgroups that display parthenogenesis, almost exclusively. However, residing within one of these clusters is the taxa Crotoniidae, which displays sexual reproduction. Based on an evolutionary analysis, a team of German researchers conclude this group re-evolved the capacity for sexual reproduction.8

The re-evolution of shell coiling in limpets. From an evolutionary perspective, the coiled shell has been lost in gastropod lineages numerous times, producing a limpet shape, consisting of a cap-shaped shell and a large foot. Evolutionary biologists have long thought that the loss of the coiled shell represents an evolutionary dead end. However, researchers from Venezuela have shown that coiled shell morphology re-evolved, at least one time, in calyptraeids, 20 to 100 million years after its loss.9

This short list gives just a few recently discovered examples of Dollo’s Law violations. Surveying the scientific literature, evolutionary biologist J. J. Wiens identified an additional eight examples in which Dollo’s Law was violated and determined that in all cases the lost trait reappeared after at least 20 million years had passed and in some instances after 120 million years had transpired.10

Violation of Dollo’s Law and the Theory of Evolution

Given that the evolutionary paradigm predicts that re-evolution of traits should not occur after the trait has been lost for twenty million years, the numerous discoveries of Dollo’s Law violations provide a basis for skepticism about the capacity of the evolutionary paradigm to fully account for life’s history. The problem is likely worse than it initially appears. J. J. Wiens points out that Dollo’s Law violations may be more widespread than imagined, but difficult to detect for methodological reasons.11

In response to this serious problem, evolutionary biologists have offered two ways to account for Dollo’s Law violations.12 The first is to question the validity of the evolutionary analysis that exposes the violations. To put it another way, these scientists claim that the recently identified Dollo’s Law violations are artifacts of the evolutionary analysis, and not real. However, this work-around is unconvincing. The evolutionary biologists who discovered the different examples of Dollo’s Law violations were aware of this complication and took painstaking efforts to ensure the validity of the evolutionary analysis they performed.

Other evolutionary biologists argue that some genes and developmental modules serve more than one function. So, even though the trait specified by a gene or a developmental module is lost, the gene or the module remains intact because they serve other roles. This retention makes it possible for traits to re-evolve, even after a hundred million years. Though reasonable, this explanation still must be viewed as speculative. Evolutionary biologists have yet to apply the same mathematical rigor to this explanation as they have when estimating the timescale for loss of function in dormant genes. These calculations are critical given the expansive timescales involved in some of the Dollo’s Law violations.

Considering the nature of evolutionary processes, this response neglects the fact that genes and developmental pathways will continue to evolve under the auspices of natural selection, once a trait is lost. Free from the constraints of the lost function, the genes and developmental modules experience new evolutionary possibilities, previously unavailable to them. The more functional roles a gene or developmental module assumes, the less likely it is that these systems can evolve. Shedding one of their roles increases the likelihood that these genes and developmental pathways will become modified as the evolutionary process explores new space now available to it. In this scenario, it is reasonable to think that natural selection could modify the genes and developmental modules to such an extent that the lost trait would be just as unlikely to re-evolve as it would if gene loss was a consequence of neutral evolution. In fact, the study of eye loss in the Mexican tetra suggests that the modification of these genes and developmental modules could occur at a faster rate if governed by natural selection rather than neutral evolution.

Violation of Dollo’s Law and the Case for Creation

While Dollo’s Law violations are problematic for the evolutionary paradigm, the re-evolution—or perhaps, more appropriately, the reappearance—of the same biological traits after their disappearance makes sense from a creation model/intelligent design perspective. The reappearance of biological systems could be understood as the work of the Creator. It is not unusual for engineers to reuse the same design or to revisit a previously used design feature in a new prototype. While there is an irreversibility to the evolutionary process, designers are not constrained in that way and can freely return to old designs.

Dollo’s Law violations are at home in a creation model, highlighting the value of this approach to understanding life’s history.


  1. Richard Dawkins, The Blind Watchmaker: Why the Evidence of Evolution Reveals a Universe without Design (New York: W.W. Norton, 2015), 94.
  2. Charles R. Marshall, Elizabeth C. Raff, and Rudolf A. Raff, “Dollo’s Law and the Death and Resurrection of Genes,” Proceedings of the National Academy of Sciences USA 91 (December 6, 1994): 12283–87.
  3. Michael Lynch and John S. Conery, “The Evolutionary Fate and Consequences of Duplicate Genes,” Science 290 (November 10, 2000): 1151–54, doi:10.1126/science.290.5494.1151.
  4. Meredith Protas et al., “Regressive Evolution in the Mexican Cave Tetra, Astyanax mexicanus,” Current Biology 17 (March 6, 2007): 452–54, doi:10.1016/j.cub.2007.01.051.
  5. John J. Wiens, “Re-evolution of Lost Mandibular Teeth in Frogs after More than 200 Million Years, and Re-evaluating Dollo’s Law,” Evolution 65 (May 2011): 1283–96, doi:10.1111/j.1558-5646.2011.01221.x.
  6. Vincent J. Lynch and Günter P. Wagner, “Did Egg-Laying Boas Break Dollo’s Law? Phylogenetic Evidence for Reversal to Oviparity in Sand Boas (Eryx: Boidae),” Evolution 64 (January 2010): 207–16, doi:10.1111/j.1558-5646.2009.00790.x.
  7. Thaddeus D. Seher et al., “Genetic Basis of a Violation of Dollo’s Law: Re-Evolution of Rotating Sex Combs in Drosophila bipectinata,” Genetics 192 (December 1, 2012): 1465–75, doi:10.1534/genetics.112.145524.
  8. Katja Domes et al., “Reevolution of Sexuality Breaks Dollo’s Law,” Proceedings of the National Academy of Sciences USA 104 (April 24, 2007): 7139–44, doi:10.1073/pnas.0700034104.
  9. Rachel Collin and Roberto Cipriani, “Dollo’s Law and the Re-Evolution of Shell Coiling,” Proceedings of the Royal Society B 270 (December 22, 2003): 2551–55, doi:10.1098/rspb.2003.2517.
  10. Wiens, “Re-evolution of Lost Mandibular Teeth in Frogs.”
  11. Wiens, “Re-evolution of Lost Mandibular Teeth in Frogs.”
  12. Rachel Collin and Maria Pia Miglietta, “Reversing Opinions on Dollo’s Law,” Trends in Ecology and Evolution 23 (November 2008): 602–9, doi:10.1016/j.tree.2008.06.013.
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Earwax Discovery Gives New Hearing to the Case for Intelligent Design



If you are like most people, you probably haven’t devoted much thought to earwax, unless it relates to the safest way to clean it out of your ears.

But earwax is worth thinking about, because it is a remarkable substance with extraordinary properties, as recent work by engineers from Georgia Institute of Technology (GIT) attests.1 In fact, the GIT researchers think that they can use their new insight about earwax to develop specialized filters for electronic devices that must perform in dusty environments.

By using earwax as an inspiration for new technology, these researchers have unwittingly provided more evidence for intelligent design, while at the same time raising a powerful challenge to the evolutionary explanation for the history and the design of life.

What Is Earwax?

This substance is an eclectic mixture of fatty acids, fatty alcohols, cholesterol, and squalene formed from secretions of the sebaceous and the ceruminous glands that line the outer portion of the ear canal. Earwax also consists of shed epithelial cells and hair.

Earwax is produced by all mammals, including humans. Two different types of earwax are found in humans, referred to as wet and dry. Honey brown in color, wet earwax contains a higher concentration of lipids and pigments than dry earwax. A single genetic change converts wet earwax (which is the genetically dominant form) into dry earwax (the genetically recessive form), which is gray and flaky.

The type of earwax a person has reflects their ancestry, with people of African and European descent having the wet variety and Asian and Native American people groups having dry earwax. Anthropologists have noted a correlation between earwax type and body odor. People with wet earwax tend to be more odiferous than people with dry earwax. Anthropologists think this correlation reflects sweat production levels, with people with wet earwax sweating more profusely than people with dry earwax. Presumably, the mutation which alters the color and consistency of the earwax also impacts sweat production. Anthropologists think that reduced sweating may have offered an advantage to Asian peoples and Native Americans, and consequently, dry earwax became fixed within these populations.

What Is the Function of Earwax?

Earwax serves several functions. One is protecting the inner ear from water, dust particles, and microorganisms. Even though earwax is a solid substance, it allows air to flow through it to the inner ear. Yet, the high fat content of earwax makes it an ideal water repellent, keeping water away from the inner ear. The hair fibers in earwax serve a useful function, forming a meshwork that traps dust particles. And the acidic pH of earwax and the lysosomes from the cellular debris associated with it impart this waxy secretion with antibacterial and antifungal properties.

The fatty materials associated with earwax also help lubricate the skin of the inner ear canal as the earwax moves toward the outer ear. Earwax motion occurs via a conveyor action set up, in part, by the migration of epithelial cells toward the outer ear. These migrating cells, which move at about the same rate as fingernails grow, carry the earwax along with them. Jaw motion also helps with the earwax movement.

By comparing earwax from several animals and by video recording earwax in human ear canals, the GIT researchers discovered that earwax has special properties that make it a non-Newtonian fluid. It is solid at rest, but flows when under pressure. Apparently, the pressure exerted on the earwax from jaw movements helps it to flow toward the outer ear. This movement serves as a cleaning mechanism, carrying the debris picked up by the earwax toward the outer ear. Interestingly, the particles picked up by the earwax alter its consistency, from a waxy material, to a flaky solid that readily crumbles, making it easier to clear the outer ear, while making room for newer, cleaner earwax.

New Technology Inspired by Earwax

The GIT engineers recognized that, based on its physical properties, earwax could serve as an inspiration for the design of new types of filters that could protect electronics from water and dusty environments. With a bit of imagination, it is possible to conceive of ways to take advantage of shear-thinning behavior to design filters that could be readily replaced with cleaner ones, once they have trapped their limit of dust particles.

Biomimetics, Bioinspiration, and the Case for Intelligent Design

It has become rather commonplace for engineers to employ insights from biology to solve engineering problems and to inspire the invention of new technologies. This activity falls under the domain of two relatively new and exciting areas of engineering known as biomimetics and bioinspiration. As the names imply, biomimetics involves direct copying (or mimicry) of designs from biology, whereas bioinspiration relies on insights from biology to guide the engineering enterprise.

From my perspective, the use of biological designs to guide engineering efforts seems fundamentally at odds with evolutionary theory. Generally, evolutionary biologists view biological systems as the products of an unguided, historically contingent process that co-opts preexisting systems to cobble together new ones. Evolutionary mechanisms can optimize these systems, but they are still kludges, in essence.

Given the unguided nature of evolutionary mechanisms, does it make sense for engineers to rely on biological systems to solve problems and inspire new technologies? Is it in alignment with evolutionary beliefs to build an entire subdiscipline of engineering upon mimicking biological designs? I would argue that these engineering subdisciplines do not fit with the evolutionary paradigm. On the other hand, biomimetics and bioinspiration naturally flow out of a creation model approach to biology. Using designs in nature to inspire engineering only makes sense if these designs arose from an intelligent Mind.


Engineers’ Muse: The Design of Biochemical Systems” by Fazale Rana (article)
Beetles Inspire an Engineering Breakthrough” by Fazale Rana (article)


  1. Society for Integrative and Comparative Biology, “The Technological Potential of Earwax,” Science News(blog), ScienceDaily, January 6, 2017,
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