The Proceedings of the Ninth International Conference on Creationism (2023)

4) Directed genetic change nullifies random mutation as the source for adaptation Evolutionary biologist Jerry Coyne reiterates a central tenet in table 1, “true, the raw materials for evolution – the variations between individuals – are indeed produced by chance mutations. These mutations occur willy-nilly, regardless of whether they are good or bad for the individual” (Coyne 2009). The purpose of our experimental tests on cavefish is to assess if that assumption is based on real observations, or is Coyne reciting some form of a creed. A substantial body of literature identifies (i) an unexpectedly large number of ways to produce adaptive phenotypes that are decoupled from random mutation altogether, and (ii) highly-regulated genetic changes that appear to be directed toward specific adaptive outcomes. These findings are not consistent with current neo-Darwinian theory (NDT). The assumption that mutational processes were disconnected with changes in environmental conditions seemed to be demonstrated in 1943 by the widely-cited Luria–Delbruck experiment. Their experiments on bacteria infected by bacteriophages was taken as proof that mutations in bacteria conferring resistance to phages existed before phage exposure (Luria and Delbruck 1943). These results have, somehow, been continuously heralded as proof that mutations are Table 2. Condensed outline of a biological research program guided by a Theory of Biological Design (TOBD). (a) A TOBD functions as an interpretive framework of biological phenomena that is part of a paradigm which presumes that organisms look engineered because they are engineered. The organisms possess a unique quality called “life” that the environment as an aggregate does not possess. Two primary research implications are that organisms are viewed as active problem-solving agents, and their environment is an unconscious set of variable conditions to which the organisms are exposed. Thus, the environment is incapable of independently exercising agency. Internalism is a major element of the framework for assumptions and interpretations within a TOBD that stands in stark contrast to the externalism of NDT. (b, green) Four core assumptions within the rationale for initiating a biological research program that is consistent with an engineering project. Engineering-based biological research is limited to explaining biological functions and does not address consciousness. (c, gray) Three basic tenets of a TOBD are descriptive of engineering principles that are essential for pursuing a correct understanding of biological operation. (d, white) The core tenets of a TOBD that constrain how observations will be characterized, and what biological research should be focused on within an engineering-based framework. (e, magenta) Major inferences from explanations of engineered systems within a TOBD. random. Their results do indicate that genetic information for resistance to phages doesn’t need to be associated with phage exposure (i.e. some bacterial populations also undergo genetic changes after exposure to phage (Foster 2004)). Yet, if a design-based explanation had been considered, then bacterial resistance prior to exposure to phages, antibiotics, or mechanisms that activate genetic change, could be interpreted to indicate that bacteria were engineered with potential solutions that existed prior to exposure to a variety of context-dependent challenges. That mutagens, copying errors, etc., are possible causes of true random mutations is not disputed by us. But, there has always been an absence of direct evidence that all mutations, especially genetic changes associated with suitable adaptations to environmental challenges, are fully random. Brundin (1986) noted this lack of evidence when stating, “The great primary problem is evidently set by the mutations. Are they random or nonrandom?” By the 1960’s some evolutionists recognized the need for nonrandom genetic changes in order for the evolutionary process to plausibly explain all that it claimed. This was due to the objective inefficacy of the random mutation-selection mechanism as Barbara Wright identified, “The existence of such mechanisms [nonrandom genetic modification] has been preBOYLE, ARLEDGE, THOMAS, TOMKINS, AND GULIUZZA Testing the cavefish model 2023 ICC 137

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