dicted by mathematicians – for example, Bernhard (1967) – who argued that, if every mutation were really random and had to be tested against the environment for selection or rejection, there would not have been enough time to evolve the extremely complex biochemical networks and regulatory mechanisms found in organisms today” (Wright 2000). In fact, the reassuring assumption that mutations occur at random has long been challenged by discoveries of molecular biology, which indicate that complex regulation of genetic change is at work. And because these findings are inconsistent with NDT, they are “ignored or side-lined”, or have been outright marginalized (Shapiro and Noble 2021, p. 147). For instance, Barbara McClintock’s discoveries in the 1940’s of transposable “controlling elements” that could control gene expression and regulate adaptation were initially ostracized, and then disregarded (McClintock 1987). In the 1970’s the SOS DNA-damage response and subsequent regulated, “inducible” genetic change mechanisms were clearly non-random processes (Witkin and George 1973; Radman 1975). Additionally, Barry Hall’s early work indicated the prosses of regulated genetic change when he found rare, yet beneficial, mutations occurring sequentially within the same bacterium (Hall and Hartl 1974; Hall 2003). More evidence of regulated genetic change was identified following John Cairns’ discovery that specific genetic changes appear in Escherichia coli only when needed (Cairns et al. 1988), and by his further proposition of “directed” or “adaptive” mutagenesis in starvation-stressed bacteria (Cairns and Foster 1991). Detailing what we currently know about specific mechanisms that produce adaptive phenotypes would fill an enormous review article. James Shapiro has broadly characterized these particular mechanisms as “natural genetic engineering” and his books link to over a thousand references (Shapiro 2022). The ‘big-picture’ shows that there is a growing body of evidence that many mutations are not random in their formation (Hogeweg 2015). In fact, many genetic changes seem to be specifically programmed as targeted responses to specific external conditions. Adaptive responses in bacteria can result from the same independently occurring genetic change in different populations (Herron and Doebeli 2013). Short segments of DNA can be inverted to generate new patterns in human chromosomes (Löytynoja and Goldman 2017). When cells detect different environmental conditions, innate mechanisms that are not completely understood can change their chromosome state and alter DNA methylation patterns (Angers et al. 2010; Zhu et al. 2013). There is strong evidence that intracellular enzymes control the locations and events of genetic changes on chromosomes in humans. (Pinto et al. 2016). Significant work by Hull et al. (2017) indicates that yeast cells appear to direct greater variation to exact locations in their genome where it would protect them against a toxin, which therefore “provides cells with a remarkable and unexpected ability to alter their own genome in response to the environment”. And, recent research on genetic changes in the plant Arabidopsis thaliana “found a lower mutation frequency inside gene bodies and certain essential genes, shattering the long-standing idea that mutations are entirely random across the genome” (Veitia 2022). However, even with increasing evidence that targeted, nonrandom genetic mechanisms are involved in the production of adaptive traits, there is persistent opposition. Futuyma (2013) insists that “genetic variation arises by random mutation and recombination”. Furthermore, he also holds to a fundamental, but now incorrect premise, that “environmental effects of an individual’s phenotype do not alter the genes passed on to its offspring” (Futuyma 2013). Both statements adhere to the assumption that directed or purposeful genetic changes don’t occur. Although the examples above (previous paragraph) do not indicate that ‘random variation and recombination’ are adequate mechanisms for generating the extensive, complex genetic variation observed in biological systems. And what about the transfer of environmentally induced genetic and regulatory effects? It is widely held that August Weismann’s lecture in 1883 established the ‘fact’ of an impermeable barrier between “disposable” cells of the soma (body) and “immortal” cells of the germline (gametes) in animals (Weismann 1889). This ‘Weismann barrier’ is a longstanding central theme of the NDT. Futuyma tells us that “extensive subsequent research has provided no evidence that specific hereditary changes can be induced by environmental conditions under which they would be advantageous (Futuyma 2013, p. 10). Yet, assertions like Futuyma’s are at least a decade out of date. We now know that epigenetic mechanisms can regulate and facilitate inheritance of the acquired characteristics of adaptive traits between parent and offspring (Jablonka 2017). Soma to germline informational transfers have been identified by several mechanisms (Sharma 2013), and chromosomes within mouse spermatozoa have been modified by interactions with non-germline DNA (Pittoggi et al. 2006). And several researchers have identified extracellular vesicles that can transfer genetic material from soma to germ cells (Eaton 2015). Furthermore, the germline descends from a somatic lineage in unicellular eukaryotes and in plants, and is designated from the soma in multicellular animals. Bacterial geneticist, James Shapiro (2022 p.16) sums up the hardened resistance of NDT theorists to incorporate this new path of research: “despite massive genomic evidence to the contrary, the philosophy of evolution by random processes – the neo-Darwinian Modern Synthesis – still reigns supreme in the public mind, in the classroom, and in the minds of many scientists and clinicians as well”. Fitzgerald and Rosenberg (2019) summarize what they and other researchers have been discovering: …but this view [random mutation] is being revised by discoveries of molecular mechanisms…these mechanisms reveal a picture of highly regulated mutagenesis, up-regulated temporally by stress responses and activated when cells/ organisms are maladapted to their environments – when stressed – potentially accelerating adaptation. Mutation is also nonrandom in genomic space, with multiple simultaneous mutations falling in local clusters, which may allow concerted evolution…assumptions about the constant, gradual, clock-like, and environmentally blind nature of mutation are ready for retirement. Our results of rapid repigmentation in the cavefish model are an indicator that depigmentation in these fish is not the product of a ‘broken’ pigmentation pathway due to random mutations. The melanin synthesis pathway is clearly functional, responsive, reversible, and therefore adaptive. Based upon a large body of literature, and our experiments thus far, the current perception that random mutations provide the genetic variation required for adaptive change, is in error. CET is a predictive and testable substitute. D) Future directions in cavefish research at the ICR Within the span of one year, the Institute for Creation Research has established three new resources dedicated to experimental research. These resources include a (1) Biology Laboratory equipped with a recirculating aquaculture system of aquaria for maintenance and experimental treatment of Astyanax mexicanus cavefish and surface fish; a (2) Molecular Biology Laboratory equipped with technology for standard and advanced protocols in molecular research, including PCR, gene cloning, riboprobe synthesis and sample preparations BOYLE, ARLEDGE, THOMAS, TOMKINS, AND GULIUZZA Testing the cavefish model 2023 ICC 138
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