Natural genetic engineering (NGE)
November 9, 2013 | James Kohl
What Natural Genetic Engineering Does and Does Not Mean by James A. Shapiro on 02/28/2013
Excerpt 1: “NGE is shorthand to summarize all the biochemical mechanisms cells have to cut, splice, copy, polymerize and otherwise manipulate the structure of internal DNA molecules, transport DNA from one cell to another, or acquire DNA from the environment. Totally novel sequences can result from de novo untemplated polymerization or reverse transcription of processed RNA molecules.”
Excerpt 2: If experiments show that cells can make distinct appropriate NGE responses to different adaptive challenges occurs, we need to figure out how they do so.
In my model, natural genetic engineering (NGE) is exemplified by the de novo creation of olfactory receptor genes that allow nutrients from the ecological niche to enter cells of unicellular and multicellular organisms. Upon entry, the nutrients are metabolized to species-specific pheromones that control reproduction. De novo creation of olfactory receptor genes leads to the de novo creation of species-specific blends of pheromones. Genetically predisposed blends of pheromones are produced but the blends are also clearly altered by receptor-mediated nutrient uptake. This enables the signaling pathway for nutrient uptake to control the pathway for reproduction. That dual control of a single signalling pathway is exquisitely fine tuned by experiences in an ever-changing environment of nutrient availability, which determines whether or not reproduction will occur in species from microbes to man. Reproduction is unequivocally non-random, nutrient-dependent, and pheromone-controlled.
For contrast with the excellent representations of biological facts that Dr. Shapiro and others have included in what are clear refutations of mutation-initiated natural selection, one aspect of these refutations that is missing. It is the physics of reproductive physiology. On 02/22/13, less than one week before Dr. Shapiro detailed what NGE means, it became clearer why that meaning must include physics. Until then, antibiotic resistance exemplified the adaptation of unicellular organisms to their environment via epigenetic changes in intercellular signaling and downstream effects on stochastic gene expression. However, the “Evolution of Escherichia coli rifampicin resistance in an antibiotic-free environment during thermal stress” is a game-changer in the context of NGE. These authors showed “…amino acid substitutions conferred different levels of rifampicin resistance.
NGE must now incorporate the thermodynamics of intercellular signaling that leads to nutrient-dependent pheromone-controlled adaptive changes via organism-level thermoregulation in species from microbes to man. Ecological, social, neurogenic, and socio-cognitive niche construction can only occur within the physical constraints of relatively narrow temperature ranges, which are also somewhat organism-specific. However, increasing thermodynamically-controlled organismal complexity clearly violates the second Law of thermodynamics. This presents what may be the final challenge to evolutionary biologists who believe in mutation-driven evolution. They must enlist biophysicists to 1) explain the violation of the second Law; or 2) eliminate physics from mutation-initiated natural selection; or 3) separate mutation-driven evolution from natural selection, or 4) admit that they have misrepresented everything they said automagically occurred in the context of adaptations to the sensory environment, which are obviously nutrient-dependent and pheromone-controlled.
The Dobzhansky–Muller incompatibility (DMI) theory was just replaced by genotype ratio distortion (GRD), which can now incorporate what is known about the biophysics of thermodynamics and thermoregulation of epistasis. GRD-associated epistasis appears to start with nutrient-dependent pheromone-controlled amino acid substitutions in Escherichia coli. The concept of GRD-associated epistasis extends to a nutrient-dependent pheromone-controlled amino acid substitution in a human population that adaptively evolved in central China, supposedly during the last ~30,000 years.
Note: It is especially interesting to see the challenge to the DMI theory come via information on GRD from researchers at Harvard et al., when the research on the amino acid substitution in a human population was reported by researchers from Harvard et al., in the context of mutation-driven evolution. We may soon see academics battle for positions that are experimentally unsupported in theory, but supported by experimental evidence in model organisms from plants to microbes to man since the molecular mechanisms appear to be conserved.