Looking Between Genes Reveals Differences by Design, Not Evolutionary Descent

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The work of our wise common Designer is evident even between our genes.

Every time a baby is conceived, his or her genetic blueprint is put to work orchestrating construction of his or her human body. Yet geneticists have found that primate animals share many of the twenty to thirty thousand protein-coding genes in the human genome. From almost the same genetic building blocks, very different results are achieved! But is that the result of evolution, or God’s design?

Believing these shared genes are the result of shared evolutionary ancestry, Adam Siepel and his team of computational biologists at Cornell University report they can analyze how natural selection reworked the genome of the ancestral ape-like animal that humans and chimps supposedly shared 4–6 million years ago to produce us.1

Carpenter Ants in Various Sizes

Through dietary adjustments in carpenter ants, McGill University scientists were able to control the expression of a single gene called EGFR, producing ants ranging in size from 1.6 to 2.5 mm in length, mimicking what happens in nature. This demonstrated one way that genetic expression can be influenced by the environment. Image reproduced from Mélanie Couture and Dominic Ouel, The Canadian Press.

Blocks and Switches

Genes that code for the construction of the proteins in an organism are like little LEGO® blocks. And each kind of living thing inherits a similar set from which to build itself. “Remarkably we use nearly the same building blocks as chimpanzees, but we end up with very different results,” computer scientist Brad Gulko explains.2 This makes sense, for biochemically speaking all living things have pretty much the same basic needs and share the same planet with essentially the same resources.

The view that Darwinian evolution works by changing protein-coding genes has proven quite implausible because changes in such genes are far more likely to be detrimental than helpful. Furthermore, only a tiny fraction of the genome consists of protein-coding genes. The Cornell team, trying to determine how evolution worked its magic over millions of years, concluded that less than ten percent (only 4.2–7.5%) of our protein-coding DNA shows evidence of evolutionary tinkering.3

But, as mentioned above, not all the DNA in the genome codes for proteins. In fact, most of it doesn’t! The Cornell team found that the functionally important parts of the human genome are 5.4 to 10.1 times more likely to be in these noncoding parts of the genome than in the coding parts.4 In other words, it appears that, from a genetic point of view, it isn’t so much the building blocks of life that make us differ but how those building blocks are used.

The Cornell team calculated that more than half of the important places distinguishing our genome from a chimp’s are “intergenic”—in between the genes. And “introns”—noncoding spacers within genes—accounted for another 35% of what makes the human genome special. They believe these are the places where evolution has been busy randomly evolving modifications on which natural selection could act.

Both intergenic regions and introns can be involved in switching genes on and off. Thus the team concludes—without commenting on how genetic information evolved in the first place—that evolution crafted us more by randomly tinkering with the way information was used than by altering the information itself.

Good “Junk”

Answers in Genesis’ molecular geneticist Dr. Georgia Purdom points out that it is completely untenable to think that in only a few million years the innumerable random changes needed to create new and increasingly complex kinds of living things could occur and then run the gauntlet of natural selection, even if “only” the flipping of genetic switches was needed:

Now evolutionists are going to have to admit that junk DNA is not junk because there aren’t enough differences in the genes for humans and chimps to be so different. The problem for evolution is how do you get that many changes in such a short period of time evoltionarily speaking?

In the past, many intergenic regions and introns like those pinpointed in the Cornell study were considered useless, functionless leftover evolutionary junk. Recent studies have shown that the vast majority of so-called junk DNA actually does have a function, as evidenced by the fact that 80% of the nucleotides in our so-called “junk” DNA are biochemically active. This of course is exactly what we would expect in a world of life designed by a wise common Designer, even after 6,000 years of the ill effects due to sin’s curse.

The Cornell team disputes the significance of junk DNA’s importance but admits they are looking at functional importance in a different way:

This finding stands in contrast to estimates that ~80% of nucleotides may be functional, based on measures of ‘biochemical activity.’ However, it is important to bear in mind that these evolutionary and biochemical estimates reflect somewhat different definitions of function, and this may explain some of the difference between them.5

Indeed the Cornell calculation of just what constitutes functional importance in the human genome is heavily influenced by evolutionary assumptions. They calculate that only 4.2–7.5% of our nucleotides are functionally important enough to have been acted on by natural selection over evolutionary time “since the divergence of humans and chimpanzees.” In order to make their calculations “as direct as possible,” the Cornell authors note that they utilized “an evolutionary model that considers sequence divergence between the human, chimpanzee, orangutan and rhesus macaque genomes.” But of course there is no way to directly calculate the effect of evolution over millions of years since such evolutionary change has never been observed and is only assumed to have occurred!

Peeking Between the Genes

While nothing about the Cornell group’s conclusions supports evolutionary claims, its report that regulatory DNA buried within and between genes governs most of the differences between primate animals and humans is borne out by another recent study from Sweden’s Karolinska Institute. Researchers there, comparing transcription factors (proteins that transcribe DNA into RNA) produced by the genomes of humans, mice, and fruit flies, found they pretty much “speak” the same language.

"We observed,” explains lead author Kazuhiro Nitta, “that, in spite of more than 600 million years of evolution, almost all known DNA words [genetic regulatory regions] found in humans and mice were recognised by fruit fly transcription factors.”6

Transcription factors influence which genes get expressed and when. They do this by interacting with the genes’ own regulatory regions. Together the transcription factors and the regulatory regions they recognize can be thought of as genetic switches.

The team pinpointed the regulatory codes recognized by the 242 transcription factors in fruit flies. Then they tried out fruit fly transcription factors on human and mouse genetic regulatory regions. The fruit fly transcription factors recognized them.

Humans do, Nitta’s team found, have some transcription factors that fruit flies lack, but only in cell types that fruit flies also lack. They concluded that evolution of the “DNA words” to which transcription factors bind was the major driving force in the evolutionary divergence of life into so many different forms. They also believe that the evolution of some novel transcription factors made even more differences in complexity possible.7

Amazing Consistency and Still Going Strong

Even the genetic switches specific to each organism are part of that genetic information that makes each organism unique. Evolutionists cannot account for the origin of the information in genes, in their regulatory elements, or in transcription factors. Observational science has yet to uncover any mechanism by which an organism can acquire the genetic information to evolve into a new, more complex kind of organism. The notion that molecules-to-man evolution has been going on for 600 million years—or has ever gone on at all, for that matter—is a Bible-rejecting worldview-based conjecture, shrouded in circular reasoning and inconsistent with biological observations.

That the same basic set of transcription factors is pretty much the same across the board does not demonstrate 600 million years of evolutionary stability—surely a very improbable notion—but rather illustrates the wisdom of our Creator God, the common Designer of all living things. Likewise, the discovery that differences between very different species rest largely in the regulatory parts of their genomes is what we would expect from a wise Creator. In fact, though evolutionists claim it is evidence of their claims, even the consistency of the genetic code—the language in which all living things “write” their instructions—is what we would expect knowing that in the beginning, about 6,000 years ago, God designed all kinds of living things to share the same planet.

Go to the Ant

Yet another recent study illustrates the genetic switching mechanisms God included in His design for living things—while never shown to produce a new and more complex kind of organism—do equip some organisms to vary within their own created kind and thereby adapt. This study, from a McGill University group, revealed why carpenter ants living in the same colony vary greatly in size. They found that 70% of the size differences in these clones descended from the same queen could be explained by whether or not a single gene—EGFR—was methylated or not. Methylation is the chemical attachment of a small group of atoms (called a “methyl” group) to a gene. DNA methylation is a well-known way that genetic expression is regulated.

“We used to think that traits like size that fall along a continuum were controlled by many, many, many genes, each having a small role, with the environment having a smoothing-out role,” explains coauthor Ehab Abouheif. Abouheif and colleagues learned that methylation of EGFR in ant larva was the deciding factor in determining adult size. “What we’ve found is something quite fundamental—by putting a coat on a single gene, you can generate that whole continuum in size. You get this chemical coating on the gene that modifies the way the gene works. You don’t need any changes in the gene.”8

Such controls on genetic expressions are called epigenetic, because they work “above” the level of the genes. Because environment can promote epigenetic changes, this mechanism equips many populations to adapt without losing any of their actual genetic information. Epigenetic changes are one way our Creator equipped living things to adapt while keeping their options open.

McGill researchers found that they could manipulate DNA methylation of EGFR using changes in dietary folate, a B vitamin. They were thus able to produce a continuum of variants from 1.6 to 2.5 mm long. “What the food is doing is affecting these chemical modifications,” explains Abouheif. “We’ve got to find out what other genes are involved, connect the dots between the food and the chemical modification. We have to see how this applies in other vertebrate systems. It’s just the beginning, really.”9

EGFR is not only regulated by DNA methylation but also controls many other genes. In honeybees, for example, EGFR influences the DNA methylation of multiple genes associated with cell growth.10 And EGFR is present in many species, including humans. As Abouheif notes, “What we’re showing is that genes and the environment are equal in their power to generate these continuous traits,” variations that do not even result in any loss of genetic information.

In their conclusion, the McGill authors call attention to the “apparent gap between the assumptions” of Darwinian genetics in its attempt to explain the origin of diverse complex living things and what genetics actually reveals. They admit, “Countless studies have demonstrated that QTLs [quantitative trait loci] cannot in themselves explain all heritable variation underlying quantitative traits, such as growth or size in humans, Arabidopsis and yeast. These difficulties underscore the many challenges that remain in understanding the genetic basis of quantitative trait variation.”11 And though they claim their work helps fill this void, it too fails to support is amoeba-to-ant evolution, or any other scenario of evolving increased complexity through random processes.

When we take a close look at the DNA that provides the blueprint to make us what we are, and to make other living things what they are, we see the hand of wise Designer who created a perfect world, with all kind of plants and animals, about 6,000 years ago. He equipped them to vary and adapt to the changing conditions in a world soon to be cursed by sin. Alterations in EGFR expression have, incidentally, been implicated in association with some kinds of cancer, a reminder that epigenetic control, like the many other good things God designed, can go wrong in this sin-cursed world.

The science of genetics cannot explain the origin of life or of genetic information in the first place. Nor can it offer a mechanism to connect the dots between different kinds of organisms. The science of genetics reveals much about the way God designed the world to function, but rather than supporting an evolutionary origins story it affirms the eyewitness account in the history book of the universe, the eyewitness account provided by the Creator God.

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Footnotes

  1. They report that their calculation “reflects time scales since the divergence of humans and chimpanzees, about 4-6 million years ago,” but add that their results are also more or less consistent with similar estimates “based on tens or hundreds of millions of years of mammalian evolution.” From B. Gulko et al., “A Method for Calculating Probabilities of Fitness Consequences for Point Mutations Across the Human Genome,” Nature Genetics 47, no. 3 (March 2015): 276–285, doi:10:1038/ng.3196.
  2. Tina Hesman Saey, “Human Evolution Tied to a Small Fraction of the Human Genome,” ScienceNews, January 19, 2015, https://www.sciencenews.org/article/human-evolution-tied-small-fraction-genome.
  3. The team calculates that only “4.2–7.5%
of nucleotides in the human genome have influenced fitness since the human-chimpanzee divergence, and they suggest that recent evolutionary turnover has had limited impact on the functional content of the genome.” From Gulko et al., “A Method for Calculating Probabilities . . . ” doi:10:1038/ng.3196.
  4. Ibid.
  5. Ibid.
  6. Kazuhiro Nitta, “Language of Gene Switches Unchanged Across Evolution,” Phys.org, March 17, 2015, http://phys.org/news/2015-03-language-gene-unchanged-evolution.html.
  7. The authors write, “Taken together, our results indicate that human and fruit fly TF [transcription factor] binding specificities display a striking level of conservation, despite dramatic morphological differences resulting from more than 600 million years of evolution and lack of detectable sequence conservation at the level of cis-regulatory elements [noncoding regions of DNA that regulate transcription of nearby genes]. These results indicate that analogously to the genetic code, which is more conserved than protein-coding DNA, the gene regulatory code is much more conserved than the regulatory sequences themselves. Our results suggest that morphological divergence is not driven by subtle drift in specificity of TFs, but primarily caused by cis-regulatory changes, with some contribution from relatively large shifts in binding specificities of specific TFs.” From K. Nitta et al., “Conservation of Transcription Factor Binding Specificities Across 600 Million Years of Bilateria Evolution,” eLife 4:e04837 (March 17, 2015), doi:10.7554/eLife.04837.
  8. The Canadian Press, “Canadian Scientists Double the Size of Ants in Experiment,” The Star (Canada), March 12, 2015, http://www.thestar.com/news/canada/2015/03/12/canadian-scientists-double-the-size-of-ants-in-experiment.html.
  9. Ibid.
  10. S. Alvarado et al., “Epigenetic Variation in the Egfr Gene Generates Quantitative Variation in a Complex Trait in Ants,” Nature Communications 6, no. 6513 (11 March 2015), doi:10.1038/ncomms7513.
  11. The authors write,

    The eventual unification of Mendelian inheritance with Darwin’s theory of natural selection was made possible by the infinitesimal model, which assumes that quantitative trait variation is generated by the action of an infinite number of loci that have small and equal effects on the phenotype. The evolution of quantitative traits is therefore thought to occur through random mutations across these loci. However, the empirical search for QTLs has revealed that trait variation often maps to specific genetic regions of small or large effect, and with specific functions. The apparent gap between the assumptions of the infinitesimal model and the results of QTL analyses is further exacerbated by the fact that countless studies have demonstrated that QTLs cannot in themselves explain all heritable variation underlying quantitative traits, such as growth or size in humans, Arabidopsis and yeast. These difficulties underscore the many challenges that remain in understanding the genetic basis of quantitative trait variation. Our findings may help resolve these outstanding challenges in the field of quantitative genetics because they show that the phenotypic possibilities of a genetic locus may be determined by both genetic variation and the influence of the environment through quantitative DNA methylation. Therefore, alongside genetic variation, the environment can generate a vast array of quantitative trait variation in natural populations.

    From Alvarado et al., “Epigenetic Variation in the Egfr Gene . . . ” doi: 10.1038/ncomms7513.

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