Tim D. Fails To Bridge Gap Between 'Micro' and 'Macro' Evolution – Again!

A few months ago, I tackled an attempt by one of our atheist regulars to bridge the gap between ‘micro’ and ‘macro’ evolution. At the time, I argued that, while Tim D. is correct on the rather elementary point that species are not static or immutable (but change or ‘evolve’ in response to environmental pressures), there is no justification for supposing that the Darwinian mechanism of adaptation can be extrapolated to explain evolution on a significantly grander scale. I showed that, while neo-Darwinian evolution possesses some explanatory power, there is empirical indication that the scope for change is not without limit.

Summarising the main points I made in my previous article:

  1. Since there is now a wealth of evidence to indicate that DNA is a necessary but non-sufficient factor in determining the morphogenesis of organismal form — that is, the animal’s body plan — there is no reason to think that mutations affecting DNA alone can be extrapolated to explain the larger-scale features of organisms such as body plan morphogenesis.
  2. Since the body plan of organisms is established right at the beginning of development, the types of changes which are required to evolve a novel body plan are the very kind which are least likely to be tolerated by organisms.
  3. Richard Lenski’s experimental work on E. coli demonstrates almost the exact opposite to what Tim D. wanted it do.
  4. Neo-Darwinism lacks the power to account for the irreducible and interlocking complexity of macromolecular machines such as the bacterial flagellum.
  5. Neo-Darwinism lacks the power to produce even seemingly trivial innovations in function where the change requires the alteration of multiple nucleotides each of which confers no selective benefit on its own.
  6. Functional protein folds are extremely rare and isolated in sequence space, and thus there is no reason to think that a blind search could stumble upon the fitness peaks given the time allowed by the age of the earth.

I thus showed that there is not only an absence of evidence for the causal efficacy of neo-Darwinism to explain all of life; but there is also an evidence of absence.

Confused About Evolution

Tim’s post is littered with confusion after confusion. One of the first concepts to get mangled is the mutationist school of evolutionary thought. Tim defines a “mutationist” as someone who “believe[s] that mutations are somehow naturally inclined toward ‘beneficiality’ or ‘directional evolution'” in contrast to “Darwinian evolutionists” who maintain that “mutations are introduced basically at random, not in any sense “directional” or otherwise biased towards improvement” But this is completely wrong. The mutationist view (which has been espoused by such key figures as Thomas Hunt Morgan, Willhelm Johannsen, William Bateson and Hugo de Vries) emphasises the creative role of mutations over and above selection.

What Tim is describing as “mutationism” here is probably closer to some forms of neo-Lamarckism which maintain that mutations arise not randomly, but in response to environmental pressures. One classic study (Luria and Delbruck 1943) is traditionally cited in these discussions in support of the traditional view that mutations occur irrespective of environmental concerns. This study involved the exposure of a strain of E. coli to bacteriophages and demonstrated that the probability distribution for the number of mutants exhibited the characteristics expected only if random mutations had been present prior to exposure to the phage, apparently ruling out the proposition that the mutations occurred as a result of the phage. That being said, there have been a number of interesting papers that have been published in recent years which report regulation of mutation rates and localised variation in response to stress (see, for instance, Galhardo et al., 2007 and Rando and Verstrepen, 2007).

A further confusion on Tim’s part pertains to his assertion that “An example of [speciation] would be if a particular population of a certain species had mutated sex cells that prevented them from forming offspring with members of other populations of that species; we would then say that this population was ‘speciated’ from all other populations.” Mutations in the germ cells which negatively affect an organism’s capacity to reproduce are not going to become fixed in any population because a key part of this process is the ability to reproduce. Does Tim really think this is a serious argument? In any case, Tim seems to think that I somehow have doubts about the occurrence of speciation; but such skepticism is harboured nowhere in my writings.

Bald Assertions

Under the heading “Macroevolution: Microevolution Times A Million”, Tim effectively does the very thing that I lamented in my previous post: He asserts that the ‘micro-‘ to ‘macro-‘ extrapolation is justified, but does not do the hard work of responding to the positive arguments I gave for thinking that it isn’t (see the non-exhaustive list of six reasons given above).

The Evidence That I Am “Wholly Unaware Of”

About half-way down his new essay, citing as his source the old beacon of reason, The Talk-Origins Archive, Tim gives us three pieces of evidence for neo-Darwinian evolution that I am allegedly “wholly unaware of”. This is a curious claim, since his third example I have already explicitly discussed in my writings (towards the end of this post). Since Tim evidently is impressed with these evidences, however, let’s discuss them in turn.

The Evening Primrose: Tim’s first example is the evening primrose, to which he assigns the out-dated species designation Oenothera gigas (though, in fairness, this was indeed the species name designated by Hugo de Vries in 1905). de Vries essentially discovered that a variant with a chromosome number of 2N = 28 (as opposed to 2N = 14) made the variant non-crossable with Oenothera lamarckiana (a name which is similarly now defunct). There are at least two reasons why this argument doesn’t wash:

  1. Polyploidy — the possession of more than two paired (homologous) sets of chromosomes perhaps as the result of chromosome doubling — is known to be a very frequent phenomenon in plants. Polyploid plants are generally unable to breed with the parent species. This is often interpreted as resulting in the birth of a new species, but the actual phenomenon is not very spectacular.
  2. de Vries had presumed that tetraploid Oenethera plants would breed true: that is to say, they would form a new and distinct species. But the plants were not able to form their own self-perpetuating populations, and generated a range of chromosome sets (diploid, triploid, tetrapoid and so on) in their progeny. In fact, the claim that the plant constituted a new species has been falsified more than six decades ago (Davis, 1943)! Indeed, Bradley Moore Davis reported, “In summary it should be emphasized that this amphidiploid did not present a settled behaviour of all pairing on the part of the chromosomes at diakinesis. On the contrary, there was much irregularity in the process of chromosome segregation during meiosis. Accounts of amphidiploids have frequently assumed that these plants even from hybrids would breed true because the double set of chromosomes would permit a regular pairing between homologues. It will be noted that here is an amphidiploid Oenothera hybrid in which the pairing is far from regular with the result that the plant does not breed true, as will appear in the accounts of later generations.”

Sea Cows: Tim explains that, “in a display of common kinship with land mammals, [sea cows] have elephant toenails on their flippers, as well as an internal skeleton that is completely homologous to humans and other terrestrial tetrapods; it contains rudimentary pelvic bones (especially odd for a creature that supposedly has, neither currently or historically, the need of a pelvic region nor a relation to any organism that does have one), yet no hind limbs.” Indeed, it is true that these sea cows possess elephant toenails on their flippers. But this only succeeds in bringing us back to the old “common features = common ancestry” argument. It is also by no means implausible that these organisms were once able to walk on land. At any rate, the manatee’s flipper is used in similar fashion to a human hand, allowing the manatee to grasp and hold objects, as well as readily bring food to its mouth. Regarding the supposed pelvic bones, this argument is justified provided the pelvic bones — which are embedded in the pelvic musculature — are truly without function. It may be an artifact of a time when sea cows once walked on land in similar fashion to a sea lion today. In sea lions, a flexible pelvic girdle facilitates easier movement on land by rotation of their hind flippers underneath their bodies.

The Origin of Chromosome 2: Tim writes that, “Apes and humans have been famously connected by the study of genetics; in human DNA, there is a strand which is exactly identical to two specific segments of an ape’s DNA. It appears to have been formed from two chromosomes that joined together at some point during our ancestry; this is made more readily apparent by the presence of two telomeres connecting together in the center of the strand — normally, telomeres are only present at the end of a strand, but this particular strand is the length of two telomeres, indicating that they were likely two separate strands that had been joined together to form a single strand with an elongated telomere at the center.” I have already linked to my previous discussion of this point. But since Tim raises it, let me briefly address it.

Briefly, the chromosomal fusion argument for human-chimp common descent begins with the observation that humans possess 23 pairs of chromosomes, whereas apes possess 24 pairs, thus allowing one to predict that — evolution being true — a chromosomal fusion must have taken place at some point in our lineage. And, indeed, this is what we observe. Chromosome 2 possesses two centromeres. It also possesses a section where there are two telomeres in the middle of the chromosome, which are oriented in such a way so as to suggest that the ends of the two chromosomes were fused together. Every telomere in human and great-ape chromosomes has the six base-pair sequence TTAGGG repeated over and over approximately fifty to one hundred times in tandem. Such telomeric repetitive units, when they are found not in the telomeres at the end of the chromosome, but rather in the middle of the chromosome (perhaps near the centromere), are referred to in the literature as “interstitial telomeric sequences” (or ITS’s). At the supposed fusion site in chromosome 2, the sequence in the upper strand abruptly changes from TTAGGG repeats to CCCTAA repeats (the complementary sequence of the inversion). This is taken to indicate that the DNA in a telomere of one chromosome and the DNA in a telomere of the other chromosome broke and subsequently the two chromosomes fused at the broken ends. This site is referred to in the literature as 2q13 (“2” referring to the chromosome number, “q” referring to the long arm, and “13” referring to the position on the arm).

Furthermore, chromosomal centromeres possess a characteristic DNA called alpha satellite sequences. Secondary alpha satellite DNA (over and above that which is associated with the active centromere), which has been found in the case of chromosome 2 (see Avarello et al. 1992), is taken as further evidence for this fusion event.

But just how sound is this argument?

For one thing, there are, in fact, plausible alternative explanations for this observation. For example, envision a scenario where our genus Homo, originally possessing 48 chromosomes, underwent a chromosomal fusion event within its own independent lineage. Sure, the banding patterns of chromosome 2 are similar to two of the autosomes in the chimpanzee lineage. But then we are only coming back to the argument from similarity which, as I have already argued, supports common descent no more than it suggests common design.

Secondly, some of the arguments for supposing that chromosome 2 did indeed arise from a fusion event have been significantly weakened in recent years. One very interesting peer-reviewed paper, appearing in the journal Cytogenetic and Genome Research in 2009, by Farre, Ponsa and Bosch, reported:

Although their function has not yet been clearly elucidated, interstitial telomeric sequences (ITSs) have been cytogenetically associated with chromosomal reorganizations, fragile sites, and recombination hotspots. In this paper, we show that ITSs are not located at the exact evolutionary breakpoints of the inversions between human and chimpanzee and between human and rhesus macaque chromosomes. We proved that ITSs are not signs of repair in the breakpoints of the chromosome reorganizations analyzed. We found ITSs in the region (0.7-2.7 Mb) flanking one of the two breakpoints in all the inversions assessed. The presence of ITSs in those locations is not by chance. They are short (up to 7.83 repeats) and almost perfect (82.5-97.1% matches). The ITSs are conserved in the species compared, showing that they were present before the reorganizations occurred.

So, what is the significance of the cited paper? Though there are many documented instances of these interstitial telomeric sequences in the genomes of humans and chimps, the 2q13 interstitial telomeric sequence is the only one that is able to be associated with an evolutionary breakage point or fusion. The other ones do not square up with chromosomal breakpoints in primates at all!As the authors of the paper note,

The availability of complete genome sequences (Hubbard et al., 2007) offers the opportunity to characterize the regions flanking the breakpoints of chromosomal reorganizations at the molecular level. However, to our knowledge, only the head-to-head ITS located in the human 2q13 region, which is a relic of an ancient telomere-telomere fusion, is precisely associated with an evolutionary breakpoint (Ijdo et al., 1991). Here, we used bioinformatic tools to analyze, in the current genome releases, the presence of short ITSs in the chromosomal inversions that do not involve terminal regions and that occurred between human and chimpanzee and between human and rhesus macaque during evolution.”

The pro-ID evolutionary biologist Richard Sternberg has also briefly weighed in on the paper here. Sternberg notes,

How, precisely, are miles and miles of TTAGGG of significance? From the standpoint of chromosome architecture, the repetitive elements en masse have the propensity to form complicated topologies such as quadruplex DNA. These sequences or, rather, topographies are also bound by a host of chromatin proteins and particular RNAs to generate a unique “suborganelle” — for the lack of better term — at each end. As a matter of fact, the chromatin organization of telomeres can silence genes and has been linked to epigenetic modes of inheritance in yeast and fruit flies. Furthermore, different classes of transcripts emanate from telomeres and their flanking repetitive DNA regions, which are involved in various and sundry cellular and developmental operations.[…]

ITSs reflect sites where TTAGGG repeats have been added to chromosomes by telomerases, that these repeats are moreover engineered — literally synthesized by the telomerase machinery, that ITSs have a telomere-like chromatin organization and are associated with distinct sets of proteins, and that many have been linked to roles such a recombination hotspots.

Thus, the take-home message is this: To make much of the 2q13 interstitial telomeric sequence and portray it as typical of what is observed in chimp and human genomes may be considered careful cherry-picking of data.And what about the secondary alpha satellite sequences found in chromosome 2? Is that not best understood as a genetic residue from a previously functioning centromere on a separate chromosome? Perhaps. But the situation is not quite as clear as is often made out. Neo-centromeres, for example, are rare human chromosomal aberrations where a new centromere is formed (see, for example, Warburton 2004). One suggestion, however, that the additional centromere in chromosome 2 did not arise by this process is the fact that neo-centromeres are usually not associated with the characteristic centromeric repetitive alpha-satellite DNA. But these neo-centromeres are poorly understood, and it may come to pass that a mechanism is discovered that can make these neo-centromeres full of alpha-satellite DNA.

One particularly interesting study, from Baldini et al. (1993), reported the presence of secondary alpha satellite DNA on human chromosome 9! To further complicate matters, Luke and Verma (1995) subsequently reported on the occurrence of secondary alpha satellite DNA in all primates. In 1997, a research group published another interesting study (Samonte et al., 1997). These researchers hybridized twenty-one different chromosome-specific human alpha satellite DNA probes to the full complement of chromosomes from the chimpanzee, gorilla and the orangutan. They reported that most of the human probes failed to hybridize to the equivalent ape chromosome. Instead, they gave positive signals on non-corresponding chromosomes. Thus, they concluded, alpha satellite DNA sequences show little conservation in primate lineages.

Confused About The Micro vs. Macro Distinction

Tim subsequently calls into question my use of the terms ‘micro-‘ and ‘macro-‘ to describe evolution, observing that the creationist group ‘Answers-in-Genesis’ repudiate the distinction on their website. I quite agree that the dichotomy is over-simplistic, and I do not often use the terms. But I was not the one to initiate use of the terms in this discussion. Moreover, in classes associated with my Masters degree in evolutionary biology, professors have used the terms “microevolution” and “macroevolution” to distinguish between small-scale within-species evolution and large-scale between-species evolution respectively. The terms have also been used in the professional literature.

Confused About Gene Duplication And The Origin Of Biological Information

Tim goes on to give us an example of an alleged case of novel biological information being added to the genome by virtue of gene duplication and subsequent mutational divergence. He writes,

…there is evidence that the four protein chains in current human adult globins actually originated from an ancestor genome which “split” around 500,000,000 years ago into two parts; each part then later mutated separately and became a different cluster. This happened again around 400,000,000 years ago, and the alpha gene mutated again, following a similar path and giving us the zeta chain. This much is actually supported by contemporary phylogenetic analysis, as well — other animals descended from those who existed around the time of the genome split (and which were associated with our ancestral line) also demonstrate this same split, and the same chromosomal arrangement of these genomes.

No, Tim, this is a retrospective analysis based on sequence homologies. At the very best, it would demonstrate common ancestry of the globin protein family (but even that conclusion is suspect). And numerous problems abound for the proposed scenario.

Consider the divergence between the alpha and beta chains of haemoglobin. Following the duplication of the initial haemoglobin gene, each copy has to diverge simultaneously, and in complementary ways in order to ensure a functional tetramer. For one thing, characteristic of haemoglobin is that both chains possess hydrophobic amino acids which are essential for the association of the subunits (this stands in marked contrast to myoglobin which, being a water soluble protein, possesses mostly hydrophilic amino acids on the outside of its folded structure).  It is conventional wisdom that the early haemoglobin may have been a monomer similar to myoglobin, which possessed exterior hydrophilic amino acids, some of which were subsequently substituted for hydrophobic amino acids when the two different chains evolved. For example, in their book, Hemoglobin: Structure, function and evolution (1983), Richard Dickerson and Irving Geis argue that some of these substitutions occurred prior to the gene duplication: That is to say, the early haemoglobin evolved into a tetramer (or possibly a dimer) prior to its diverging into the alpha and beta chains. Such a suggestion is, however, suspect in light of the fact that one might expect to see these hydrophobic amino acids in similar positions if they arose prior to the divergence of the haemoglobins. But the hydrophobic amino acids on the exterior of the polypeptides are different and are located in different positions on the alpha and beta chains. This promotes their complementarity: Hydrophobicity is not required in the same place for each respective polypeptide, but only at those sites which make contact with the other chains. The alpha chains are unable to make contact with one another, unlike the beta chains which are. When the beta chains are not produced (as in beta-thalassaemia, a condition which is often fatal), the unassociated alpha chains typically degrade. In the case of alpha-thalassaemia, however, where it is the alpha chains which are lacking, the beta chains do associate. This presents a different difficulty, for they bind oxygen with an affinity similar to that of myoglobin. This means that the oxygen will not be released to the tissues — again, with fatal consequences.

Given the plethora of pathological disorders which may be attributed to a change in just one amino acid in these chains (thus disrupting chain cooperativity), it should be quite evident that many amino acids in both chains are essential for the correct functioning of tetrameric haemoglobin. Moreover, many of the amino acids which are involved in this interaction are located at different positions in the polypeptide sequences (or different amino acids are found at analogous positions).

Thus, as I hope to have shown above for our current case study (i.e. the globins), for gene family trees to considered credible, it is necessary to show that there is a sufficiently high likelihood of all of the ancestral sequences conferring some sort of selective advantage. But it has been shown time and again that getting from one set of conserved amino acids to another — as is necessary for the production by divergence of proteins with different functions — is too big a jump through sequence space.

Globins possess a heme group which contains iron. Iron exists in two oxidised forms, namely Fe2+ and Fe3+(ferrous and ferric  forms respectively). When oxygen is available, the iron is readily oxidised to ferric Fe3+. But, crucial to its physiological role, the iron which is present in haemoglobin and myoglobin exists in the ferrous oxidation state. In chapter 2 of their book to which I previously alluded (Hemoglobin: Structure, function and evolution), Dickerson and Geis observe that “The purpose of the heme and the polypeptide chain around it is to keep the ferrous iron from being oxidized (metmyoglobin, with a ferric iron, does not bind oxygen), and to provide a pocket into which the oxygen can fit.”

The ferrous iron, in haemoglobin and myoglobin, is actively prevented from being oxidised to the ferric form by the the specific chemical groups of the surrounding amino acid residues. Dickerson and Geis describe the fragility of this system as follows:

“The met [oxidised] forms were experimentally the easiest to obtain, and the deoxy states also could be crystallized and studied with careful eperimental techniques. The oxy forms proved more intractable: Unless extreme care is taken, O2 oxidises the heme iron from Fe2+ to Fe3+ rather than simply binding, thus yielding the unwanted met form of the molecule.”

As one might expect, the amino acids which surround the heme group are evolutionarily highly conserved. Moreover, many pathological conditions arise as the result of changing just one amino acid, resulting in the consequential inability of the polypeptide to retain the heme group correctly, thus permitting the iron to oxidise. In many cases, changing just one amino acid alters the positioning of the amino acids next to the heme group, such that they are no longer able to protect it from oxidation. This means that the altered amino acids need not even be in particularly close proximity to the heme group!

Furthermore, while it is one thing to look at the sheer difficulty of globin evolution, the situation becomes even more bleak when one considers that the duplication to provide myoglobins and haemoglobins must have occurred at least twice in the jawless fish and in jawed vertebrates. From early on, it was concluded (from amino acid sequence comparisons) that the earliest globins were monomeric and thus led to the predominantly monomeric haemoglobins of the various invertebrate lines (e.g. insects, molluscs, jawless fish) and that only after this did the globin gene give rise to the separate myoglobin and haemoglobin of the jawed vertebrates. But the presence of myoglobin has been documented in lamphrey, a jawless fish (Romero-Herrera, 1979)!

There is, in fact, a number of examples like this. Another example is the alleged split resulting from the duplication of the alpha and beta chains to give rise to the embryonically-expressed zeta and epsilon chains. In birds, one can find similar embryonically-expressed haemoglobin chains called pie and rho. It is widely thought that the divergence dates extremely anciently, preceding the split of the lineages leading to mammals and birds.

While the zeta and epsilon chains, though similar to each other, are markedly different from the alpha chains, modern epsilon and rho chains exhibit far higher levels of similarity to mammalian and bird beta chains respectively. It may thus be concluded that the split to give rise to these embryonic versions has occurred independently on at least two occasions — in each of the mammalian and avian lines.

Finally, there is the whole issue of the regulation of gene expression. For example, the function of Myoglobin is to act as a storage of oxygen, retaining it inside the heart and skeletal muscles. This job is made possible by its higher affinity for oxygen than that of Haemoglobin. Now, the modifications of the protein’s amino acid sequence, in order for it to be converted from haemoglobin to myoglobin, would have needed to be accompanied by complementary changes in its regulatory sequences in order to ensure that the myoglobin was produced in the muscle where it is needed, rather than in bone marrow where the red blood cells are produced. Myoglobin present in red blood cells would not provide a selective advantage. In fact, it would be harmful to the organism because it would bind too tightly to oxygen and not release it to the tissues (as in the case of alpha-thalassaemia described above). This is one of the most neglected points in discussions concerning gene duplication and family trees. Another example of this is the purported duplication of the Beta chain to give rise to the gamma foetal version which possesses a higher affinity for oxygen. Such a scenario would, of course, have had to happen in concert with complementary changes in gene control such that it is expressed during pregnancy but synthesis of the Beta chain is suppressed until birth.

Confused About ID and Common Ancestry

Tim remarks,

“….I have to say, I don’t quite understand how he can say that common ancestry is ‘perfectly compatible’ with intelligent design, yet without major evolutionary change. What he calls “macroevolution” is  commonly understood to be the primary vehicle for common ancestry! If common ancestry is demonstrable, but not by evolution, then by what method does he mean to imply that all life on earth evolved from a common ancestor? It seems mutually exclusive to say that all life we see today, in all its magnificent diversity, could have come from a common ancestor *without* major evolutionary change along the way. I’m interested in his explanation for this.”

I would have thought that this is a very elementary point. Universal common ancestry represents a pattern — a pattern of hereditary continuity. But common ancestry is not, in and of itself, a causal process. Common descent could be correct but the neo-Darwinian mutation/selection mechanism totally wrong. Since ID — in its purest sense — only claims to be able to detect patterns in nature which are best explained as the product of an intelligent cause, the theory is silent on the issue of common ancestry. What ID does challenge is the materialistic view of evolution which envisions the origins and development of life on earth as being the product of the mindless and impersonal forces of nature. The key point on which proponents of ID are united is the view that the origins of life and earth have a profoundly teleological basis. ID proponents, however, disagree over issues like common ancestry. Some, like Michael Behe, accept common ancestry. Others, like myself, tend to be more skeptical.

Confused About Irreducible Complexity

On the bacterial flagellum, amazingly, Tim cites a paper (Nguyen et al., 2000) which demonstrates the very opposite from the line of argument he wishes to take! The paper suggests “that the flagellar apparatus was the evolutionary precursor of Type III protein secretion systems.” So that research is not much use to Tim’s case (which requires that the flagellum evolved from the Type-III secretion system). Moreover, flagellin monomers are somewhat potent cytokine inducers. If you are a Yersinia organism in possession of a Type-III secretion system, the last thing you want to do is display those flagellin peptides to the macrophages. Such would be liable to significantly countermand the Yersinia‘s anti-inflammatory strategy.

Tim then treats us to a proposed scenario for the flagellum’s evolution by Nick Matzke — a model which is just as overly simplistic as the one proposed by Ian Musgrave (which I mention in my article on the subject). It trivialises the sheer molecular complexity of the flagellum’s assembly apparatus.

Moreover, similarity of sequence or similarity of structure between proteins does not imply that it is easy (or even possible) for one protein to evolve into another. In fact, the protein evolution literature in general shows that unless a protein starts out with at least some level of activity for the target function, it may be impossible to convert it to that target by stepwise mutation and selection (I discuss this a little bit in my previous response to Tim).


In summary, then, Tim D. has offered us little more than he did last time — more evidence for “microevolution”, more unsubstantiated assertions and various extremely weak arguments. Again, Tim’s article promises to deliver but sends us away empty handed. Perhaps, in his next rebuttal, Tim will actually present to us the evidence which he describes here as “massive”. I live in hope…

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