Genetic Phylogeny

Sean D. Pitman M.D.

Updated © October, 2004

        Current animal and plant classification models are fairly subjective in how they are set up.  Scientists had hoped that the newer science of molecular biology would provide more objectivity to classification systems.  It was hoped that comparisons of the nucleotides of DNA or RNA sequences or of amino acid sequences in proteins would yield more consistent results that could be used to classify organisms with a high degree of accuracy.  However, according to an article in the January 1998 issue of Science:

  Animal relationships derived from these new molecular data sometimes are very different from those implied by older, classical evaluations of morphology. Reconciling these differences is a central challenge for evolutionary biologists at present. Growing evidence suggests that phylogenies of animal phyla constructed by the analysis of 18S rRNA sequences may not be as accurate as originally thought. Inaccuracies may occur in molecular phylogenies for a variety of reasons.

  Prior to analysis, the sequences of corresponding genes from each animal must be placed in register (aligned) with each other so that homologous sites within each sequence can be compared. However, sequence divergences may be sufficiently large that unambiguous alignments cannot be achieved, and different alignments may lead to different inferred relationships. Additionally, the data are often sufficiently noisy that there may be a lack of strong statistical support for important groupings. ¹

 

The article then discusses a figure detailed similarities and differences in 18s rRNA sequences which show that mollusks (scallops) are more closely related to deuterostomes (sea urchins) than arthropods (brine shrimp).  Of course, this is not too surprising.  Intuitively, a scallop seems more like a sea urchin than a shrimp.  So, the 82% correlation between the scallop and sea urchin is not surprising.  However, in this light it is surprising is that a tarantula (also an arthropod) has a 92% correlation with the scallop.  Here we have two different arthropods, a shrimp and an tarantula.  How can a scallop be much more related to one type of arthropod and much less related to the other type of arthropod? This troubling thought led the authors of the Science article to remark:

Different representative species, in this case brine shrimp or tarantula for the arthropods, yield wildly different inferred relationships among phyla. Both trees have strong bootstrap support (percentage at node). . .  The critical question is whether current models of 18S rRNA evolution are sufficiently accurate to successfully compensate for long branch attraction between the animal phyla. Without knowing the correct tree ahead of time, this question will be hard to answer. However, current models of DNA substitution usually fit the data poorly . . . ¹

There are many other interesting little problems concerning commonly used phylogenic tracing genes and proteins.  For example, mammalian and amphibian "luteinizing hormone – releasing hormone" (LHRH) is identical.  However, birds, reptiles, and certain fish have a different type of LHRH.  Are humans therefore more closely related to frogs than to birds?  Not according to standard evolutionary phylogeny trees.   Again, the data does not match the classical theory in this particular situation.¹⁵

Calcitonin (lowers blood calcium levels in animals) is another protein commonly used to determine phylogenies.  Interestingly though humans differ from pigs by 18 of 32 amino acids, but by only 15 of 32 amino acids from the salmon.  Are we therefore more closely related to fish than to other mammals like the pig? ⁵  

  Cytochrome c is another famous phylogenic marker protein used to determine evolutionary relationships.  There is only a single amino acid difference between human and chimp cytochrome c.  Because of this, many assume that the evolutionary link is obvious.  However, with many other animals, this link is not so obvious.  For example, the cytochrome c protein of a turtle is closer to a bird than it is to a snake and a snake is closer to a human (14 variations) than it is to a turtle (22 variations).⁵  Humans and horses, both being placental mammals, are presumed to have shared a common ancestor with each other more recently than they shared a common ancestor with a kangaroo (a marsupial).  So the evolutionist would expect the cytochrome c of a human to be more similar to that of a horse than to that of a kangaroo.  Yet, the cytochrome c of the human varies in 12 places from that of a horse but only in 10 places from that of a kangaroo.⁵ Such discrepancies between traditional phylogenies and those based on cytochrome c are well known.  Ayala commented that:

    “The cytochrome c phylogeny disagrees with the traditional one in several instances, including the following: the chicken appears to be related more closely to the penguin than to ducks and pigeons; the turtle, a reptile, appears to be related more closely to birds than to the rattlesnake, and man and monkeys diverge from the mammals before the marsupial kangaroo separates from the placental mammals.” ⁸  

Even so, cytochrome c does seem to generally match the predictions of common decent.  However, there are some who think that the general cytochrome c data presents some puzzles from a neo-Darwinian perspective.  First, the cytochromes of all the higher organisms (yeasts, plants, insects, fish, amphibians, reptiles, birds, and mammals) exhibit an almost equal degree of sequence divergence from the cytochrome of the bacteria Rhodospirillum.  In other words, the degree of divergence does not increase as one moves up the scale of evolution but remains essentially uniform.  The cytochrome c of other organisms, such as yeast and the silkworm moth, likewise exhibits an essentially uniform degree of divergence from organisms as dissimilar as wheat, lamprey, tuna, bullfrog, snapping turtle, penguin, kangaroo, horse, and human. ^{5, 6} According to Michael Denton, a molecular biology researcher, "At present, there is no consensus as to how this curious phenomenon can be explained." ⁷ However, there are in fact very good explanations for this phenomenon.  Consider the following data chart that compares the percent homogeny of cytochrome c among various creatures:

In reviewing this chart, pay particular attention to the tetrahymena.  Tetrahymena are unicellular ciliated protozoans.  Obviously then they would have evolved before the other creatures on the chart - according to standard evolutionary thinking.  One might then expect, as Michael Denton noted, that those creatures which are progressively more evolved would be progressively different in their cytochrome c differences as one moves up the chart.  Notice how this is not the case.  All of the creatures on this chart are approximately equidistant from tetrahymena.  Does this finding contradict the predictions of the theory of common decent?  Actually, it does not contradict the theory of common decent.  Michael Denton was mistaken in ever thinking that it did.

According to the theory of common decent, all creatures living today are equally separated in time from their first common ancestor (ie: single celled bacteria).  Even the bacteria that remain alive today have sustained mutations over time as they maintained their similar morphology.  Thus, one should expect and not be surprised when there is equal divergence between "simple" and "complex". 

It can be thought of as spokes on a wheel with the central hub being the common ancestor and the tips of each spoke representing a different creature.  The tip of each spoke is equally distant from the wheel hub as well as many of the other spoke tips on the wheel.  So obviously then, even if the tip of one of the spokes was a single celled creature, like tetrahymena, this creature would be expected to be equally distant from almost every other creature on that wheel to include other single celled creatures as well as multi-celled creatures like fish, corn, rabbits and humans.  Higher organisms, on the other hand, might be more similar to each other due to a more recent separation from a common ancestor between them.  For example, humans and chimps are both equally different from bacteria, but when compared with each other, their cytochrome c proteins are almost identical.  Thus, a more recent common ancestor seems quite logical.  Humans and chimps simply share the same wheel spoke except that this spoke splits at the very tip with humans and chimps sharing different tips.

So, the data does seem to generally match the theory even if specific anomalies may be encountered on relatively "rare" occasions in such cases as cytochrome c phylogenies.  However, there might be a few problems with this scenario definitively supporting the theory of common decent.  One problem might arise when one considers that mutation rates are calculated on a per generation average.  Consider that the average mutation rate for a given gene in all creatures, is about 1 x 10^-6 mutations per gene per generation.  That means that a given gene will mutate only one time in one million generations on average.  Consider that single celled organisms have a much shorter generation time than multi-celled organisms on average.  For example, the bacteria E. coli have a minimum generation time of 20 minutes compared to the generation time of humans of around 20 years.  With a gene being mutated every 1 to 10 million generations in E. coli, one might think this would be a long time.  However, each and every gene in an E. coli lineage will get mutated once every 40 to 80 years.  So, in one million years, each gene will have suffered at least 10,000 mutations.  

Now, cytochrome c phylogenies are generally based on analysis of certain subunits of cytochrome c which range in number of amino acids up to a maximum of about 600 or so.  This would translate into a minimum of at least 1,800 nucleic acids in DNA coding for this subunit of cytochrome c protein (3bp per codon).  Note that in the table above, the tetrahymena species are about 50% different from all other creatures on the table.  It seems then that all the creatures would have experienced at least a 25% change in their genetic codes from the time of common ancestor.  So how many generations would it take to achieve this 25% difference? 

Taking 25% of 1,800 give us 450 mutations.  Lets say that the average mutation rate is one mutation per 1,800 nucleic acids per one million generations.  For a steady state population of just one individual in each generation it would take about 450 million generations to get a 25% difference from the common ancestor.  With a generation time of 20 minutes (ie: E. coli), that works out to be about 342,000 years.  So, for bacteria, the 25% difference from the common ancestor cytochrome c, might have been achieved relatively rapidly given the evolutionary time frame. (See additional addendum comments below) 

The question is then, if bacteria can achieve such relatively rapid neutral genetic drift, why are they not more wide ranging in their cytochrome c sequences?  It seems that if these cytochrome c sequence differences were really neutral differences, that various bacterial groups, colonies, and species, would cover a rather large range of possible cytochrome c sequences - potentially to include that of mammals.  Why are they then so uniformly separated from all other "higher" species unless the cytochrome sequences are functionally based and therefore statically different due to the various functional needs of creatures that inhabit different environments? 

For example, bacteria are thought to share a common ancestor with creatures as diverse as snails, sponges, and fishes.  The split from the common ancestry of the creatures is thought to have happened over 3 billion years ago.  Then, about 600 million years ago there was the Cambrian explosion where all the major phyla of living things are thought to have suddenly evolved. So, obviously all of these creatures have all been around long enough and are diverse enough to exhibit quite a range in cytochrome c variation.  Why then are their cytochrome c sequences so clustered and arranged in such an orderly hierarchy?  Why don't bacteria, snails, fish, and sponges cover a more random range of cytochrome c sequence variation if these variation possibilities are in fact neutral? 

I propose that the clustered differences that are seen in genes and protein sequences, such cytochrome c, are the result of differences in function that actually benefit the various organisms according to their different individual needs.  If the differences were in fact neutral differences, there would be a vast overlap by now with complete blurring of species' cytochrome c boundaries - even between species as obviously different as humans and bacteria.  Because of this, sequence differences may not be so much the result of differences due to random mutation over time as they are due to differences in the functional needs of different creatures.  I think that the same can be said of most if not all phylogenies that are based on genotypic differences between all living things.

For example, consider that if either humans or bacteria would be better served by a different sequence for a particular function this different sequence would be rapidly evolved - especially in bacteria.  If the human sequence for cytochrome c would better serve E. coli bacteria than their current fairly similar type of cytochrome c, how can an evolutionist say that E. coli would have very much trouble at all evolving the human sequence?  The fact that the sequences remain consistently different over a significant span of real time observation (over a million generations for bacteria at least) is very good evidence that the differences in DNA character sequencing are based in differences of functional need, not evolutionary heritage. 

In this line consider the fairly recent comments from Elizabeth Pennisi in a 1999 Science article entitled, "Is it Time to Uproot the Tree of Life?"  

     "A year ago, biologists looking over newly sequenced genomes from more than a dozen microorganisms thought these data might support the accepted plot lines of life's early history. But what they saw confounded them. Comparisons of the genomes then available not only didn't clarify the picture of how life's major groupings evolved, they confused it. And now, with an additional eight microbial sequences in hand, the situation has gotten even more confusing . . . Many evolutionary biologists had thought they could roughly see the beginnings of life's three kingdoms . . . When full DNA sequences opened the way to comparing other kinds of genes, researchers expected that they would simply add detail to this tree. But "nothing could be further from the truth," says Claire Fraser, head of The Institute for Genomic Research (TIGR) in Rockville, Maryland. Instead, the comparisons have yielded many versions of the tree of life that differ from the rRNA tree and conflict with each other as well . . . " ¹⁰

Such problems were not completely unexpected.  Earlier, in 1993, Patterson, Williams, and Humphries, scientists with the British Museum, reached the following conclusion in their review of the congruence between molecular and morphologic phylogenies:

     As morphologists with high hopes of molecular systematics, we end this survey with our hopes dampened.  Congruence between molecular phylogenies is as elusive as it is in morphology and as it is between molecules and morphology. . . .  Partly because of morphology’s long history, congruence between morphological phylogenies is the exception rather than the rule.  With molecular phylogenies, all generated within the last couple of decades, the situation is little better.  Many cases of incongruence between molecular phylogenies are documented above; and when a consensus of all trees within 1% of the shortest in a parsimony analysis is published structure or resolution tends to evaporate.²

In 1998 biologist Carl Woese, an early pioneer in constructing rRNA-based phylogenetic trees, lamented the problem by writing:

 “No consistent organismal phylogeny has emerged from the many individual protein phylogenies so far produced.  Phylogenetic incongruities can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves. . . Clarification of the phylogenetic relationships of the major animal phyla has been an elusive problem, with analyses based on different genes and even different analyses based on the same genes yielding a diversity of phylogenetic trees.” ⁹

In 1999 Philippe and Forterre wrote an article entitled, "The rooting of the universal tree of life is not reliable" in which they made the following comments:

   "The addition of new sequences to data sets has often turned apparently reasonable phylogenies into confused ones. . . In general, the two prokaryotic domains were not monophyletic with several aberrant groupings at different levels of the tree. Furthermore, the respective phylogenies contradicted each others, so that various ad hoc scenarios (paralogy or lateral gene transfer) must be proposed in order to obtain the traditional Archaebacteria-Eukaryota sisterhood."  ¹⁶

Another 1999 Science article by Stiller and Hall:

    "A precipitous acceptance of such widespread LGT places evolutionary biologists in the untenable position of adopting an unfalsifiable hypothesis, at least in terms of the techniques of comparative sequence analyses that currently dominate the field of molecular evolution. Any phylogenetic pattern inferred from any given gene can be fit to some suitable mix of conventional intraspecies gene transmission and interorganismal genetic promiscuity. Thus, unless more reliable evidence is uncovered, the scientific method requires that we invoke the idea of ubiquitous LGT only as a last resort." ¹⁷

And another 1999 Science article by Doolittle:

"Each new prokaryotic genome that appears contains dozens, if not hundreds, of genes not found in the genomes of its nearest sequenced relatives but found elsewhere among Bacteria or Archaea." ¹⁸

Just one more 1999 paper by Ann Miller, from the Yale Department of Molecular Biophysics and Biochemistry, entitle, "The Evolution of Phylogenetic Classification: From 16S rRNA to the Genomic Tree."  

"The 16S rRNA tree is not an organismal phylogenetic tree; it is a gene tree. To move towards organismal phylogeny, scientists began creating trees based on other proteins. In many cases, the other phylogenies do confirm the rRNA tree, but no one consistent phylogeny has emerged." ¹⁹

Consistent hierarchies, at least for the earliest branches of the supposed "Tree of Life", are falling apart with additional evidence.  When a given organism has hundreds of genes which none of its supposed nearest evolutionary relatives have, evolutionists are left in a very perplexing position.  In order to maintain their theory they must propose, in an ad hoc non-falsifiable manner, that these differences were not the result of evolution from a common ancestor over time, but were in fact the result of lateral transfer of pre-evolved sequences.  This messes the notion of nested hierarchies up very badly as far as its being a "science" is concerned.  It is not science since it is not falsifiable.  It is nothing more than "just so" story telling. 

But what about the higher branches that do show a more consistent nested hierarchical picture?  It may be true that the higher branches do show a more nested hierarchical pattern, but the discovery of a lack of such a pattern at lower branches has not removed the notion that evolution was still responsible.   So, evolutionary mechanisms are used to explain both hierarchical and non-hierarchical patterns.  No matter how high up the tree this lack of hierarchy goes, the theory of evolution would still be used to explain the origin of such patterns.  For focal problems in the tree between branches at higher levels, a change in mutation rate, or notions like convergence, divergence, or even lateral gene transfer are used.  The fact is that the theory of evolution cannot be falsified by either a universal or a focal lack of nested hierarchy.  Beyond this, the hierarchical classification method was first introduced by creationists, not evolutionists.  So, to say that hierarchical patterns, when present, definitely support the the theory of evolution over intelligent design theory is erroneous.  The theory of evolution does not predict hierarchical patterns more than does intelligent design theory.  Again, nested hierarchies can be found all the time in human designs. 

However, the death knell to this whole thing is the fact that most of these phylogenetic trees are based on functional genetic sequences.  That messes everything up.  Evolutionists would have a much stronger case if the sequences in question were actually neutral with regard to phenotypic function, but they aren't.  That is why the notion of "pseudogenes" was so popular for such a long time - until recently when pseudogenes were actually found to be functional. What this means is that the differences are clustered or nested because of the different functional needs of different organisms in different environments. 

Many types of functional proteins shared between very different creatures, like cytochrome c, are quite similar overall.  In fact, certain key positions are highly conserved.  The differences are also quite interesting in that they are maintained over thousands and even millions of generations.   This means that most of the differences for such sequences are not neutral, but are indeed functional. In such a protein, that is otherwise so similar, it wouldn't take much to get to a new sequence if the new sequence was more functionally beneficial or "optimal". 

Some argue that this doesn't happen because the different sequences are equally beneficial or "optimal" if applied to the same organism. That is basically arguing that the differences are not in fact functional different, but are actually neutral with respect to a functional optimum.  Again, that makes no sense in light of the evidence that the differences, in addition to the similarities, are maintained over time.  If this neutral argument were correct, then the distribution of sequences would be more randomly distributed. In other words, it would not be so neatly nested. 

The evidence of functional maintenance over time is very strong evidence that the nested differences are not so much the result of common ancestry as they are the result of various functional needs of different organisms in different environments.  The more different the overall phenotype combined with the overall environment, the more different one can expect the individual sequences of a great many genes and proteins to be.  And, this is pretty much what we find in real life.

 Others have attempted to counter by suggesting that whales and dolphins should then be more similar to fish than to mammals since they live in the water instead of on land.  Of course, the problem with this suggestion is that environment is not the only thing that plays into various genetic functional optimums.  The other genes and the overall phenotype of the organism must also be considered.  We should not expect the cytochrome c sequence of a dolphin to be the same a shark just because they both live in the same environment and eat many of the same things.  Why? Because they have very different overall phenotypes.  Also, we should not expect the cytochrome c sequence of a dolphin to be the same as that of a cow just because they are both classified as "mammals".  Why?  - Because they occupy very different environments and have a just a few differences in overall phenotype as well. 

Even modern humans, when occupying different environments, will evolve different genetic sequences for various protein products that are actually functionally maintained over time due to various advantages that the differences provide in the different environments.  There are many examples of this.  And yet, when placed in the same environment, the differences quickly disappear in the offspring over time.  Why?  Because, there are indeed different optimal sequences when different overall phenotypes interact with different environments.

So again, I propose that the significant majority of differences between the cytochrome c of bacteria and humans are functional. They are not neutral.  If the human sequence were put in a bacterium, it might survive ok, but it would not do as well.  Over time, its offspring would rapidly evolve back the original more optimum sequence. 

So far, the evidence is in fact far more consistent with the notion of common design with functional maintenance over time.  It is starting to look a great deal like the books on my bookshelf or like the various types of cars on the highway - quite a few similarities combined with a great many distinct and isolated differences.

Hominid/Primate D-loop Sequence Analysis

 

 

       A "few million years" might also be a problem for the resolution of mitochondrial D-loop sequences.  Consider that the sequences used (two of them) to estimate the time of the most recent common ancestor (MRCA) between modern humans, Neandertals, and chimpanzees where each less than 400 base pairs in length (333bp and 340bp respectively).  The mutation rate used by Krings et. al. was based on the a priori assumption that modern humans split off from chimps some "4-5 million years" ago.  Based on this perhaps plausible, but indirect assumption, a substitution rate of 0.94 x 10^-7 substitutions per site per year per lineage, was determined.  Using this rate, the MRCA between humans and Neandertals was calculated to have lived about 465,000 years ago.  The MRCA of modern humans was calculated to have lived around 163,000 years ago.  And, the MRCA of chimps and bonobos was calculated to have lived around 2,844,000 years ago. ^{3, 11, 13} 

       Krings' figures are all fine and good except if we happen to come across a more direct measurement of mtDNA mutation rates.  Consider the following work by Thomas Parsons published in the journal Nature Genetics:

 

       "The rate and pattern of sequence substitutions in the mitochondrial DNA (mtDNA) control region (CR) is of central importance to studies of human evolution and to forensic identity testing. Here, we report a direct measurement of the intergenerational substitution rate in the human CR. We compared DNA sequences of two CR hypervariable segments from close maternal relatives, from 134 independent mtDNA lineages spanning 327 generational events. Ten substitutions were observed, resulting in an empirical rate of 1/33 generations, or 2.5/site/Myr. This is roughly twenty-fold higher than estimates derived from phylogenetic analyses. This disparity cannot be accounted for simply by substitutions at mutational hot spots, suggesting additional factors that produce the discrepancy between very near-term and long-term apparent rates of sequence divergence. The data also indicate that extremely rapid segregation of CR sequence variants between generations is common in humans, with a very small mtDNA bottleneck. These results have implications for forensic applications and studies of human evolution . . .

       The observed substitution rate reported here is very high compared to rates inferred from evolutionary studies. A wide range of CR substitution rates have been derived from phylogenetic studies, spanning roughly 0.025-0.26/site/Myr, including confidence intervals. A study yielding one of the faster estimates gave the substitution rate of the CR hypervariable regions as 0.118 +- 0.031/site/Myr. Assuming a generation time of 20 years, this corresponds to ~1/600 generations and an age for the mtDNA MRCA of 133,000 y.a. Thus, our observation of the substitution rate, 2.5/site/Myr, is roughly 20-fold higher than would be predicted from phylogenetic analyses. Using our empirical rate to calibrate the mtDNA molecular clock would result in an age of the mtDNA MRCA of only ~6,500 y.a., clearly incompatible with the known age of modern humans. Even acknowledging that the MRCA of mtDNA may be younger than the MRCA of modern humans, it remains implausible to explain the known geographic distribution of mtDNA sequence variation by human migration that occurred only in the last ~6,500 years." ¹²

 

 

       Several other more recent real time studies dealing with historical families have backed up Parson's findings.  So, it seems as though more direct real-time measurements of mtDNA mutation rates show as much as a 20-fold higher mutation rate than that which was used by Krings et al.  Now what does this mean - besides the obvious? 

        The sequences studied by Krings totaled 673 base pairs in length.  According to the rate determined by Parsons, every single one of these base pairs would have changed more than twice in one million years and at least once in 400,000 years.  Half of the base pairs would have mutated at least once in 200,000 years.  And yet, humans are separated by only about 95 or so substitution differences from chimps?  What is wrong with this picture?  Each substitution difference (in a sequence some 673 base pairs in length) takes an average of 600 years to achieve.  Taking into account that each lineage would build up substitution differences separately, in 600 years there would be around two substitution difference between two lineages.  This seems to indicate that the common ancestor of humans and chimps lived some 30,000 years ago (not 4 to 8 million years ago as Krings et al., suggest - based on indirect methods).  Modern humans, being separated from each other by an average of only 10 substitutions (according to Krings), appear to have a common ancestor living some 3,000 years ago.  Modern Humans and Neandertals are separated by an average of only 35 substitutions.  This seems to indicate a common ancestor living only some 10,000 years ago. 

 

 

 

The Most Reasonable Explanation

 

“It should be noted that molecular phylogenies are constructed on the basis of certain evolutionary assumptions.  The tree that is presented is chosen from a forest of alternatives, typically on the assumption of maximum parsimony.  That is, the tree that is selected is the one that reflects the least amount of presumed evolutionary change.  But, if the assumption of maximum parsimony fails to fit the data, it can be jettisoned in favor of another.”⁴  In other words, any result can be accommodated by the theory by revising one or more of the underlying assumptions.

Even if a morphological phylogeny was matched closely by multiple molecular phylogenies, that would not prove that the groups in question descended from a common ancestor.  The molecular differences could be linked to the morphological differences for some other reason.  For example, all of the living organisms on this planet live in a relatively similar environment.  All use the same water, breathe the same air, and eat the same basic foods for building blocks and energy.   Is it not reasonable to assume that a similar environment requires at least some similarities in the creatures that utilize it for survival? 

Consider a world were plants utilized a different type of amino acid for protein metabolism than animals.  This would mean that animals could not eat plants because the amino acids for one metabolic system would not necessarily work in the other system.  The animals in such a world would be left with nothing to eat except for each other.  The fact that creatures have many of the same or similar genes and proteins means that they are integrated with each other in their environment common environment (i.e., Earth).  If they were not, they could not survive.  Similar proteins and metabolic pathways are needed to utilize similar sources of food and energy.  The various parts of organic life on this planet are interchangeable, not because of some random happenstance, but because of necessity - like Lego blocks.  Building blocks not made by the Lego company will not “work” with Lego blocks. 

Nothing lives to itself.  All living things are dependent upon other living things.  If they were not molecularly and thus genetically compatible, nothing would survive very long.  The “cycle of life” is dependent upon this fact.  There would be no cycle if the basic building blocks of the creatures involved were not interchangeable with each other.   Considering this need, it seems reasonable to assume that those creatures that share the most similar environments, body plans, and physiology would also have the most similar needs and thus the most similar genetic and molecular machineries.  

Biologist Leonard Brand makes this point quite eloquently in the following excerpt:

      “Anatomy is not independent of biochemistry.  Creatures similar anatomically are likely to be similar physiologically.  Those similar in physiology are, in general, likely to be similar in biochemistry, whether they evolved or were designed…  An alternate, interventionist hypothesis is that the cytochrome c molecules in various groups of organisms are different (and always have been different) for functional reasons.  Not enough mutations have occurred in these molecules to blur the distinct grouping evident.  If we do not base our conclusions on the a priori assumption of megaevolution, all the data really tell us is that the organisms fall into nested groups without any indication of intermediates or overlapping of groups, and without indicating ancestor/descendant relationships.⁵

 

    So, classification models of living things that are based on molecular similarities and differences are quite limited as far as their use as evidence of common ancestry beyond very recent times.  Many differences that are maintained seem to be function based.  Because of this, certain differences in sequences cannot be used as a "molecular clock" since natural selection fixes certain sequences based on functional needs so that random drift is not allowed.  Beyond this, very different phylogenetic relationships can be hypothesized depending upon which sequence is subjectively chosen for analysis.  These different trees are often outright incompatible with each other or, at best, inconclusive.

1. Maley, Laura E. and Charles R. Marshall. 1998. The Coming of Age of Molecular Systematics. Science Vol. 279 Issue 5350, p.505-506. ( Link to Full Text )

2. Patterson, Colin, and others. 1993. Congruence Between Molecular and Morphological Phylogenies. Annual Review of Ecology and Systematics 24:153-188.

3. Krings, M., Geisert, H., Schmitz, R., Krainitzki, H., and Pääbo, S.  DNA sequence of mitochondrial hypervariable region II from the Neandertal type specimen. Evolution, Proc. Natl. Acad. Sci. USA, Vol. 96, pp. 5581-5585, May, 1999.

4. Hunter, Cornelius G. 2001. Darwin's God: Evolution and the Problem of Evil. Baker, Grand Rapids, MI.

5. Brand, Leonard. 1997. Faith, Reason, and Earth History. Andrews University Press, Berrien Springs, MI.

6. Davis, Percival and Dean Kenyon (editors). 1993. Of Pandas and People, second edition. Haughton Publishing Co., Dallas.

7. Denton, Michael. 1998. Nature's Destiny. Free Press, New York.

8. Ayala, Francisco J. 1978. The Mechanisms of Evolution. Scientific American 239:56-69.

9. Woese, Carl. 1998. The Universal Ancestor. Proceedings of the National Academy of Sciences USA 95:6854-6859.

10. Elizabeth Pennisi, Is It Time to Uproot the Tree of Life? Science, vol. 284, no. 5418, 21 May 1999, p. 1305

11. http://www.harunyahya.com/mediawatch_99_myth_is_dead_sci34.html

12. http://www.pnas.org/cgi/content/full/96/10/5581

13. Parsons, Thomas J. A high observed substitution rate in the human mitochondrial DNA control region, Nature Genetics vol. 15, April 1997, pp. 363-367

14. Krings M., Capelli C., Tschentscher F., Geisert H., Meyer S., von Haeseler A. et al. (2000): A view of Neandertal genetic diversity. Nature Genetics, 26:144-6.

15. JA King and RP Millar, Comparative aspects of luteinizing hormone-releasing hormone structure and function in vertebrate phylogeny, Endocrinology, Vol 106, 707-717 ( Link to Abstract )

16. Philippe H, Forterre P., "The rooting of the universal tree of life is not reliable." J Mol Evol. 1999 Oct;49(4):509-23. ( Link to Abstract )

17. John W. Stiller, Benjamin D. Hall, "Lateral Gene Transfer, Genome Surveys, and the Phylogeny of Prokaryotes" Science, Vol 286, Issue 5444, 1443 , 19 November 1999 ( Link to Text )

18. W. Ford Doolittle, Science 286, 1999

19. Ann L. Miller, "The Evolution of Phylogenetic Classification: From 16S rRNA to the Genomic Tree." Department of Molecular Biophysics and Biochemistry, New Haven, CT, 1999 ( Link to Text )  

Addendum:

The mutation rate for humans is estimated to be about 2.2 x 10^-9 mutations per base pair per year. With about 6.3 billion base pairs per genome, that works out to around 14 transmissible mutations per year per person. 

By random chance alone in a *neutral* sequence we would expect to see 25% identity and 75% non-identity between two DNA sequences.  We could achieve this "random look" with only 50% of each of two DNA sequences undergoing random mutation.  So, how long would it take for 50% of a neutral 1000 character DNA sequence to get mutated?  Well, it would take about 2.2 million years for each mutation or about 1.1 billion years for a random look.

But, what happens if the sequence is not functionally neutral?  Well, now the population size, reproductive rate, and generation time comes into play.  Given a population of say, 1 billion individuals, just about every character in our 1000-character sequence will get mutated every year in the population as a whole. A beneficial mutation will be spread throughout the population more or less rapidly depending upon the degree of its beneficial nature.  Sex allows for the genetic recombination of the most advantageous mutations thus preferentially clustering them and making it appear that the random mutation rate was higher than it really was.  Also, one mustn't forget about the oft touted "lateral gene transfer" theory, which is equivalent to sex in bacteria (and other creatures).

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. Methinks it is Like a Weasel                                                 . The Cat and the Hat - The Evolution of Code   

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. The God of the Gaps                                                           . Rube Goldberg Machines  

. Evolving the Irreducible                                                     . Gregor Mendel  

. Natural Selection                                                                  . Computer Evolution  

. Which Came First                                                                 . Antibiotic Resistance  

. The Immune System                                                            . Pseudogenes  

. Genetic Phylogeny                                                                . Fossilized DNA  

. DNA Mutation Rates                                                            . Donkeys, Horses, Mules and Evolution  

. The Fossil Record                                                                . The Geologic Column  

.  Early Man                                                                                . The Human Eye  

. Carbon 14                                                                              . Radiometric Dating  

.  Quotes from Scientists                                                           . Ancient Ice

 . Meaningful Information                                                           . Limited Evolutionary Potential

 . Harlen Bretz

Debates:

Stacking the Deck

God of the Gaps

The Density of Beneficial Functions

All Functions are Irreducibly Complex

Ladder of Complexity

Chaos and Complexity

Confusing Chaos with Complexity

Evolving Bacteria

Irreducible Complexity

Scientific Theory of Intelligent Design

A Circle Within a Circle

Crop Circles

Mindless vs. Mindful

Single Protein Functions

BCR/ABL Chimeric Protein

Function Flexibility

The Limits of Functional Flexibility

Functions based on Deregulation

Neandertal DNA

Human/Chimp phylogenies

Geology

The Geologic Column

Fish Fossils

Matters of Faith

Evidence of Things Unseen

The Two Impossible Options

Links to Design, Creation, and Evolution Websites

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