Biological variation is, in part, transmitted from parent to progeny. Tall individuals tend to have tall offspring, fast individuals tend to have fast offspring, and so forth. This transmission process is key to the action of natural selection. Those trait variations that are successful in transmitting themselves to the next generation, by definition, survived while those that failed would disappear from the population. So long as traits are transmitted, evolutionists argue that natural selection is inevitable.

In other words, whatever it is that determines your traits is also transmitted to your offspring. Therefore, if you have evolutionarily successful traits then you will have more offspring, and they will receive your successful traits.

But how are the traits defined and transmitted? Darwin didn’t quite know how but in the twentieth century it seemed obvious—via the genes. According to the merger of modern genetics and evolution, it was all in the genes. They determined your traits and they were passed on to your offspring. This view fit evolutionary theory and was quickly accepted as an unquestionable scientific fact.

There is only one problem: it is false.

The fact that our genes are practically identical with the chimpanzees genes should have been a sign to evolutionists that their gene-centric view was problematic. How could the chimp and human be so different if their genes are so similar? Nonetheless, evolutionists proclaimed the great similarity as evidence that there must be an evolutionary relationship between humans and chimps.

In fact the biological evidence is clear: genes are only part of a far more complicated story than what evolution envisioned. As Stuart Newman explains:

Genes, which are composed of DNA, directly specify the sequences of RNA molecules and indirectly, the amino acid sequences of proteins. Before there were multicellular forms, single-celled organisms evolved for as much as two billion years driven, in part, by genetic change, as well as by establishment of persistent symbiotic relationships among simpler cells. During this entire period no cellular structure or function was specified exclusively by a cell’s genes. The protein and RNA molecules produced by cells associate with each other in a context-dependent fashion or, in many cases, catalyze chemical reactions (generating lipids, polysaccharides and other molecules), whose rates depend on the temperature and composition of the external environment. So the population of molecules inside the cell can vary extensively even if the genes do not.

It was long believed that a protein molecule’s three-dimensional shape, on which its function depends, is uniquely determined by its amino acid sequence. But we now know that this is not always true—the rate at which a protein is synthesized, which depends on factors internal and external to the cell, affects the order in which its different portions fold. So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous influence over their functions.

The deployment of information in the genes, moreover, is itself dependent on the presence of certain RNA and protein molecules in the cell. Since, as described above, the composition of the cell’s interior and the activity of many of its proteins depend on more than just the genes, the portion of the genes’ information content that is actually used by the cell is determined, in part, by non-genetic factors. So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used. Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent.

As Newman explains, the gene is nothing close to how evolution envisioned it. The gene myth is yet another example of evolution’s failed expectations. It seems that inevitably evolution’s interpretations turn out to be wrong as it has produced a steady stream of false predictions. Evolution is certainly the best counter indicator in the life sciences.

We continue to examine the work of authors George Johnson and Jonathan Losos in their biology textbook, The Living World ((Fifth Edition, McGraw Hill, 2008). In their chapter on evolution and natural selection, these accomplished evolutionists begin by (1) misrepresenting the relationship between microevolution and macroevolution and biological variation here, (2) making a non scientific, metaphysical, truth claim that mandates the truth of evolution here, (3) making the false statement that the fossils themselves are a factual observation that macroevolution has occurred here and here, and (4) making a series of misrepresentations by carefully selecting the evidence to provide to the student and protecting it with circular reasoning here.

Johnson and Losos’ next move is to distort the molecular evidence. They write:

A series of evolutionary changes thus implies a continual accumulation of genetic changes in the DNA. From this you can see that evolutionary theory makes a clear prediction: organisms that are more distantly related should have accumulated a greater number of evolutionary differences than two species that are more closely related.

But how are species judged to be “distantly related”? By what measure are species compared? The answer, of course, is by the similarities and differences in their visible anatomy. So what exactly is this powerful evolutionary prediction? It is that genetic differences between species are proportional to the differences in their visible anatomy. If two species look alike, then their genomes should be similar. If they look very different, then their genomes should be very different. This is by no means a heroic prediction.

There is, however, another problem with this prediction. Aside from not being heroic, it is false. By now the authors have established a trend of misrepresentation and distortion, and predictably the trend continues:

This prediction is now subject to direct test. Recent DNA research, referred to in section 15.3, allows us to directly compare the genomes of different organisms. The result is clear: for a broad array of vertebrates, the more distantly related two organisms are, the greater their genomic difference.

Here the distortion is mainly one of omission. Like saying that geocentrism’s prediction that the planets should travel across the sky is true without mentioning retrograde motion, Johnson and Losos fail to mention important deviations from this pattern that have even evolutionists acknowledging the evolutionary expectation has failed.

Yes, there is a broad pattern of correlation between visible anatomy and molecular sequences, but there are inescapable and significant deviations which are far outside evolution’s “noise” level. If evolution predicts that “organisms that are more distantly related should have accumulated a greater number of evolutionary differences than two species that are more closely related” then evolution is false, end of story.

The authors next discuss the protein evidence, and in like manner continue their distortion:

This same pattern of divergence can be clearly seen at the protein level. Comparing the hemoglobin amino acid sequence of different species with the human sequence in figure 17.7, you can see that species more closely related to humans have fewer differences in the amino acid structure of their hemoglobin. … Again, the prediction of evolutionary theory is strongly confirmed.

Again, this prediction is not only not “strongly confirmed,” it is in fact false. Yes, hemoglobin and many other proteins fall into the non heroic pattern, but other proteins do not. These are well known to scientists, but evolution has unfortunately compromised science.

Johnson and Losos end this misleading section on the molecular evidence for evolution with yet another fallacious icon of evolution, the molecular clock.

In science theory evaluation is a critical skill. It is crucial to take a neutral, unbiased perspective and be willing to acknowledge both pros and cons of even one’s cherished theories. Unfortunately evolutionists don’t follow this scientific dictum. Yes there is plenty of evidence for evolution, but there are problems as well. But one would never know it from reading the evolution genre. Don’t count on evolutionists to give a scientifically accurate evaluation of their theory. Religion drives science, and it matters.

You probably learned in high school biology class that the new DNA data has powerfully confirmed evolution. Take any gene and it reveals differences between the species exactly as we would expect. And this sentiment is not limited to high school textbooks. As the Chair of a university Biology department once wrote to me, “DNA sequences provide an absolute and irrefutable record” that evolution is a fact. “Virtually every single gene sequence we examine,” he explained, “can be seen to be represented in closely related species and in more distantly related species with increasing numbers of nucleotide changes as we look at more distant species.” It was, he concluded, “absolute proof, in hard copy, reiterated in every single gene of every single organism.” That is an unfortunately common misrepresentation of the data but the story doesn’t end there. The DNA evidence has falsified several other evolutionary predictions.

Vast stretches of identical DNA segments are found in distant species. Multitudes of differences are found in the DNA of cousin species. Retroviruses that were so often considered to be junk now must be viewed crucial to evolutionary history if Darwin was right. These are some obvious surprises that DNA offered up to evolutionists, but there are more subtle contradictions. One of them, which shows up repeatedly, is the way DNA interacts with proteins.

Consider a recent study of how transcription factor binding is not conserved between mice and men. Transcription factors are proteins that bind to DNA and influence which genes are expressed (transcribed). You may recall that proteins are created by first transcribing genes. So in this complex regulatory network, genes are transcribed to create transcription factor which then return to regulate gene expression.

Evolutionists believe their theory is crucial to biology. Nothing in biology makes sense, they say, except in the light of evolution. We know what questions to ask and where to look only because we have Darwin’s powerful ideas guiding and motivating our research. But transcription factors in the mouse and human do not follow the evolutionary pattern.

Not only do these transcription factors often bind to retrovirus sections of DNA—which evolutionists so often considered to be nothing more than worthless junk—they also usually do not bind in the same DNA locations in spite of their importance. As one commentary explained:

Remarkably, they find that the genomic locations of binding sites for two key regulatory proteins (OCT4 and NANOG) are poorly conserved across species, despite their functional importance in mammalian embryonic stem cell biology. […]

Unexpectedly, only ~5% of binding sites for the two transcription factors OCT4 and NANOG were found in orthologous positions in human and mouse ES cells, suggesting major differences in genome-wide binding profiles between species.

And the story becomes even more contradictory with many of the binding sites were found in non conserved junk DNA:

Remarkably, many of these RABS [repeat-associated binding sites] were found in lineage-specific repeat elements that are absent in the comparison species, suggesting that large numbers of binding sites arose more recently in evolution and may have rewired the regulatory architecture in embryonic stem cells on a substantial scale.

Furthermore, even those genes with conserved transcription factor binding often revealed more detailed differences in the particular binding location:

However, among genes whose OCT4 dependence was conserved between human and mouse, most of the OCT4 binding sites identified were not directly conserved. Instead, the disappearance of a binding site in one species was compensated for by the emergence of a new binding site for the same transcription factor nearby.

The commentary concludes that these findings are consistent with other recent lineage-specific findings:

The notion that some regulatory networks have substantially changed in evolution is also supported by recent independent observations of lineage-specific network rewiring in vertebrate preimplantation embryos and adult liver tissue.

Of course there have been no observations of "network rewiring," lineage-specific or otherwise. This is yet another unfortunate misrepresentation of science. Yes, the new findings are consistent with other recent findings that species differ in subtle yet dramatic ways. But none of this was expected by evolutionary theory. As the paper explains:

Together, these results suggest that many genes have been rewired into the core regulatory network of human embryonic stem cells following the insertion of transposable elements.

So species-specific studies are required:

In contrast, OCT4 and NANOG have very different binding profiles in human and mouse embryonic stem cells, with only ~5% of their sites being homologously occupied. The fact that there is also a limited concordance between regions experimentally observed to be bound and conserved elements, as determined from multispecies sequence alignments, implies that in vivo maps in the relevant species will be important in the study of many mammalian systems. Moreover, to help explain the vast occupancy differences, we showed that species-specific transposable elements have been an important source of new sites in both species.

In other words, evolution doesn’t help explain the findings. What is remarkable is how evolutionists are able to fit even contradictory evidence into their thinking:

we were also able to identify a group of human-specific target genes that show evidence of having been added to the core regulatory network of human embryonic stem cells via the insertion of transposable elements. Although we do not expect all binding events to directly influence gene expression, this data adds important support to a seminal hypothesis on the impact of repeats on the evolution of transcription regulation.

A seminal hypothesis? That is how evolutionists describe unfounded speculation that invokes serendipity to explain unexpected findings.

Genes added to the core regulatory network via the insertion of transposable elements? This is a remarkable example of how evolution has compromised both science and the peer review process. They conclude:

Our results reveal the striking plasticity of the core regulatory network of mammalian embryonic stem cells and the importance that transposable elements have had in facilitating this functional turnover.

This is what happens when evolution is mandated as true. Religion drives science and it matters.