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This article was originally published as a chapter in the book “Design and Catastrophe: 51 Scientists Explore Evidence in Nature"
Epigenetics generally refers to phenotypes and processes that are transmitted to other cells and sometimes to future generations, but are not the result of differences in the sequence of DNA bases. Epigenetic effects are caused by changes in gene expression resulting from changes in chromatin or other aspects of the structure of genetic material. Often, these changes occur in response to the environment, food, and even to social interactions.[1]
A fundamental precept of evolutionary biology is that natural selection acts on phenotypes determined by the variation of the DNA sequence in natural populations. However, advances in understanding gene regulation have elucidated a spectrum of epigenetic molecular phenomena capable of profoundly altering temporal and spatial patterns of gene expression without changing the sequence of bases in the DNA.
The best understood mechanism of epigenetic change is DNA methylation, which refers to the addition of methyl groups to the nucleotide bases. In eukaryotes, the predominant type of DNA methylation is the methylation of cytosine to produce 5-methylcytosine. This is associated with inhibition of transcription and often occurs in the cytosine bases that are immediately adjacent to guanine nucleotides, called CpG dinucleotides. In the CpG dinucleotides, the cytosine nucleotides in the two DNA strands are diagonal in relation to each other (see Figure 38-1).
Throughout my academic training I have always been taught that random mutations are the source of genetic variability upon which natural selection operates. With rare exceptions, the literature shows this mechanism acting slowly. However, in the last two decades, many papers have challenged this paradigm by showing that epigenetic mechanisms are involved in very rapid phenotypic changes that are inherited by the offspring. In the evolutionist worldview, the terminology “selected for” or “selected against” is used to describe the survival or demise of an organism. This use mistakenly seems to ascribe primary causality to the environment as if it were imposing its will through a mystical or undetectable event of selection.[2] However, there is a difference between the naturalist worldview and the design-based worldview that shifts primary causality to the preparation of genetic and epigenetic systems designed to respond to environmental changes. These systems were designed to produce self-tuning organisms and fill environments with the creation of new ecological niches in virtually every place on Earth.
Representative examples highlight innate genetic systems in all the diverse taxonomic groups demonstrating successful characteristics in determining whether an organism survives in a new environment. These systems consist of elaborate networks of genes that have the information to help organisms address environmental challenges in real time. One component of these innate genetic systems is molecules called “chaperones,” which help to fold proteins in the right way. The concentration of these molecules can be proportional to the stressful exposures found by multicellular organisms, and their concentration directly affects the expression of significant characteristics in such a way that their modulation can either reveal or hide the phenotypic effects of natural variation. Chaperones have been implicated as a major factor in significant morphological changes such as the loss of eyes in a kind of cave fish, Astyanax mexicanus.[3] On the basis of fundamental interactions of the sensor system, these fish can feel water conductivity ranging up to five times more in caves compared to surface currents. Embryos from fish that grow under conditions of low conductivity positively regulate the genes of chaperone molecules.
Darwin’s finches, which inhabit the Galápagos Archipelago, constitute an iconic model for studies of speciation and adaptive evolution. In an attempt to verify species changes in real time, two renowned researchers conducted a study for 30 uninterrupted years between 1972 and 2001 on one of the Galápagos Islands to study Darwin’s finches.
Between 1976 and 1977, they verified that body and beak size of the finch Geospiza fortis decreased between 1984 and 1986; beak shape for this same species became thinner and remained so for the next 15 years. A different finch, Geospiza scandens, showed a gradual and uniform decrease in beak size and a rectilinear trend in beak shape, converging with the morphological characteristics of the Geospiza fortis beak. The researchers found that periods in which finches showed more marked changes in morphology and beak size were the same in which there was rain scarcity and changes in composition of the supply of seeds.[4]
The neo-Darwinian model of evolution requires random mutations to generate the phenotypic variation necessary for natural selection to act. However, what process provoked the morphological alterations of the finches’ beaks observed in short periods of environmental stress? Epigenetic inheritance has been shown to be a good model to explain gene expression patterns that have generated phenotypic differences in finches and their offspring,[5] but such hereditary changes are not associated with mutations, recombination, or anything associated with the nucleotide sequence. Rather, they are simply associated with the activation and/or inactivation of genes.
The examples presented above illustrate the innate capacity for self-tuning as a basic characteristic of all living things. These remarkable observations show us the design of organisms created to fill the earth with its dynamic and challenging environments. Therefore, the field of epigenetics offers great opportunity for creationists to develop research that demonstrates evidence for design and helps to strengthen faith in the Creator.
NOTES
[1] BA Pierce. Genetics—a conceptual approach. 7th ed. New York: W.H. Freeman; 2019.
[2] RJ Guliuzza, R Lane. A response to “Does natural selection exist?”: creatures’ adaptation explained by design-based, organism-driven approach: Part 1. Answers Research Journal 2014; 7:403–420.
[3] N Rohner, DF Jarosz, JE Kowalko, M Yoshizawa, WR Jeffery, RL Borowsky, S Lindquist, CJ Tabin. Cryptic variation in morphological evolution: HSP90 as a capacitor for loss of eyes in cavefish. Science 2013; 342 (6164):1372–1375. doi:10.1126 / science.1240276.
[4] PR Grant, BR Grant. Unpredictable evolution in a 30-year study of Darwin’s finches. Science 2002; 296:707–711.
[5] MK Skinner, C Gurerrero-Bosagna, MM Haque, EE Nilsson, JAH Koop, SA Knutie, DH Clayton. Epigenetics and the evolution of Darwin’s finches. Genome Biology and Evolution 2014; 6(8);1972–89. doi:10.1093/ gbe/evu158.
Wellington dos Santos Silva is a retired professor of human genetics and science and religion at the Bahia Adventist College. He earned a PhD in Human Genetics from the University of Brasília and a postdoctoral degree from the medicine and health program at the Federal University of Bahia. His main area of research is sickle cell disease in Afro-descendant populations in the State of Bahia, Brazil, a subject on which he has published several peer-reviewed articles. After his retirement, he continues to be involved in the creationist community in his country.