Generally, Jonathan and his audience were skeptical of macro-evolution and common descent. We discussed what Intelligent Design is, and what it is not; and how ID relates to evolution. I insisted that macro-evolution demands a higher view of God… a God that does not have to keep coming back and introducing new life forms on earth.
As I say in Evolution 2.0: “Darwinists underestimate nature. Creationists underestimate God.”
Midway through the show, a caller asked about epigenetics.
Layman’s explanation of epigenetics from Evolution 2.0:
In the Dutch famine of 1944 during World War II, thousands of unborn children experienced harsh deprivation, which resulted in unexpected changes. Not only were the children who were in utero during the famine smaller; when these children grew up and had children, their children were also smaller than average. Over their lifetime, the children of the famine experienced far-above-average rates of obesity, type 2 diabetes, cardiovascular problems, and other diseases related to an unhealthy body weight.
This data suggests that the famine experienced by the mothers triggered epigenetic changes that were inherited by the next generation.
Epigenetics doesn’t just alter the metabolism of children conceived in times of famine, though. It controls the expression of every cell in your body. The reason you have hair on the top of your head and not your forehead is because epigenetic factors control the expression of hair differently in different areas of your skin. It’s also the reason identical twins with identical DNA can still have different allergies, intelligence, aptitudes, and even different inherited diseases.
Epigenetics is blade #3 of the Evolution 2.0 Swiss Army Knife. It’s a switch that “grays out” genes, altering DNA’s function without changing the DNA sequence itself. It produces different cell types in fetal development; it alters tissues based on the external environment, and passes learned traits to offspring.
I suggested to her that it may be possible for epigenetic changes to become hard-coded into the genome over time, so that temporary adaptations become permanent. She challenged me on this. I promised to get back to her. Here’s what I found.
First, some further explanation of epigenetics, from Evolution 2.0:
I can take a sentence and make it say the opposite of what it said before, just by selectively “graying out” words and phrases:
Flight 6429 was delayed from Chicago to Winnipeg so it will not be departing before 6:45 P.M.
Flight 6429 was delayed from Chicago to Winnipeg so it will not be departing before 6:45 P.M.
(“Flight 6429 was from Winnipeg.”) Flight 6429 was delayed from Chicago to Winnipeg so it will not be
departing before 6:45 P.M. (“Flight 29 to Winnipeg will depart before 6.”)
This illustrates how Epigenetics works—by “graying out” DNA sequences and making them silent. The mechanism that grays out the code is called methylation.
So… can this temporary graying-out of genes (which happens all the time, in response to external threats – things like callouses, temperature swings and a thousand other things) become hard-coded and permanent? Is epigenetics a powerful force for long-term evolution?
From correspondence with James Shapiro of the University of Chicago:
You are describing the fascinating but mysterious phenomenon discovered by Waddington known as “genetic assimilation.” Waddington treated Drosophila embryos to induce epigenetic changes producing flies with two pairs of wings (Bithorax).
After doing this for a few generations and mating the phenotypically altered flies, he discovered he no longer needed to treat the embryos. They had acquired Bithorax mutations in their genomes!
I’m not sure this has been replicated, and I’m not aware whether the mutations were ever subjected to detailed analysis. Nonetheless, Waddington’s observations have been widely cited and gained broad credibility from his status as the father of modern epigenetics.
Epigenetics is the interface between the organism and its environment.
See Shapiro’s 2011 book Evolution: A View from the 21st Century for a broader explanation of how cells rewrite their genomes in response to a dynamically changing environment.
…how extensive, and how stable, is the information carried in the germline by the epigenome? Several known examples of epigenetic inheritance demonstrate that it has the ability to create selectable traits, and thus to mediate Darwinian evolution. Here we discuss the possibility that epigenetic inheritance is responsible for some stable characteristics of species…
Differentially expressed versions of a single allele have the potential to create an undetermined assortment of phenotypic novelties. Moreover, this increased phenotypic variation, observed within only a few generations, has the potential to play an important role in long-term evolutionary change, accelerating population divergence and driving speciation.
Methods for incorporating the parameterization of epiallelic instability in order to accurately reflect the variability of germline epigenetic modifications have no been established. These theoretical models have revealed how transgenerational epigenetic inheritance has the potential to profoundly affect usual evolutionary trajectories and result in elevated levels of phenotypic variation that would otherwise be unaccounted for under a standard population-genetic model. It has therefore been proposed that the Mendelian model requires amending in order to accommodate the transmission of “soft inheritance” alongside traditional genetic inheritance.
Although DNA methylation has been the focus of most of this research, many stably inherited epigenetic variants are believed to be caused by small RNAs, or perhaps a combination of different interacting epigenetic mechanisms. These data suggest that the composition or level of RNA in germ cells or associated cells could lead to a partial retention of epigenetic states down generations – through a combination of transmission stability and maternal effects…
From Epigenetics and Evolution by Mendizabal, Keller, Zeng and Soojin
The epigenome constitutes the interface between an organisms’ genome and its environment. Environmental factors such as chemicals, nutritional factors, or pathogens can alter the epigenetic landscape. A well-known example is how nutrition can determine the caste system in honey bees (Kucharski et al. 2008)
From: Friend or Foe: Epigenetic Regulation of Retrotransposons in Mammalian Oogenesis and Early Development by Alexei Evsikov, Caralina Marín de Evsikova
Bridging the realms of genetics and epigenetics, transposons are genetic elements regulated by epigenetic factors at biochemical and molecular levels.
TEs [Transposable Elements, discovered by Barbara McClintock] bridge genetic and epigenetic landscapes because TEs are genetic elements whose silencing and de-repression are regulated by epigenetic mechanisms that are sensitive to environmental factors. Ultimately, transposition events can change size, content, and function of mammalian genomes. Thus, TEs act beyond mutagenic agents reshuffling the genomes, and epigenetic regulation of TEs may act as a proximate mechanism by which evolutionary forces increase a species’ hidden reserve of epigenetic and phenotypic variability facilitating the adaptation of genomes to their environment.
…in mammalian genomes, experimental evidence supports epigenetic regulation of transposons as being critical to initiate synchronous, temporal expression of genes in germline, early embryos, and stem cells…
…living organisms developed and continue reinventing mechanisms for TE silencing, mostly via epigenetic mechanisms, which spares removal of TE loci from their genome…
TRANSLATION: Epigenetics gives an organism an ability to switch on a reserve of hidden programmed responses. Transposable Elements change the expression of genes and closely interact with epigenetic changes to coordinate adaptations to a constantly changing environment. Epigenetic switches can silence TEs and alter gene expression.
From Epigenetic Inheritance and Its Role in Evolutionary Biology: Re-Evaluation and New Perspectives by Warren Burggren:
In a few more extreme, yet illustrative examples, epigenetically-inherited phenotypes caused by RNA interference persist across as many as 50 generations in Caenorhabditis elegans [34,58,110,111]. In the plant toadflax, epigenetically-inherited phenotypes are said to persist across possibly hundreds of generations . Thus, the mere persistence of a modified phenotype across as many generations as most investigators have the patience to wait for is in and of itself insufficient evidence for the fixation of epigenetically-modified traits into the genome. Yet, there is evidence and theoretical arguments for both the direct and indirect involvement of epigenetics altering the genome, as will now be considered.
Confounding the determination of the role of epigenetics in evolution and speciation is the key question of whether epigenetically-acquired phenotypic traits themselves can actually become fixed intact, i.e. permanently added to the genome, as opposed to having the markers that generate them have indirect influence on the subsequent genome through genome destabilization, mutation, natural selection or other mechanisms. Mechanisms by which this might occur are emerging, but evidence remains somewhat circumstantial [4,19,27,119].
Importantly, it is not required for the epigenetically-inherited phenotype to become fixed into the genotype to affect the evolution of traits.
TRANSLATION: Epigenetic changes can extend 50-100+ generations without becoming hard-coded into the genome! This doesn’t mean the hard coding doesn’t ever happen, and there are both anecdotal indications and mathematical models to suggest it does. In any case, epigenetic factors undoubtedly affect long-term evolution.
I very commonly find that Intelligent Design advocates have a knee-jerk reaction against the power of epigenetics, transposition, symbiogenesis etc to produce large scale changes.
This opposition puzzles me. Why? Because the capabilities of such mechanisms do not, per se, undercut the general ID proposition that there is ultimate intelligence involved. But intelligence is found in the cells themselves and this makes the entire question vastly more interesting. It makes it possible for natural forms of id (lower case i, lower case d) to offer testable hypotheses that can be scientifically verified.
It seems ID people are looking for the hand of God in differences between species. But the ability for organisms to engineer new species in response to their environment is far more impressive than a God who has to repeatedly inject new forms of life into the earth.
So… given how limited our models of these systems presently are, we can only benefit by giving each adaptive process the benefit of the doubt and studying how it works – as evidenced by the fact that this very question stands at the bleeding edge of current scientific knowledge. Seeing how it took me many hours to compile just the information you see here, there is much productive work to be done.
Instead of opposing evolution scientists, why not join in and help?
ID advocates, I invite you to stop standing skeptically with your arms crossed. Instead, delve into these fascinating topics of research. In them you will find the mysteries of life.