Their paper1, published in PLoS ONE on 21 October, is the culmination of a decade of work. It presents 25 mitochondrial DNA mutations that reliably separate the two groups.
“The species concept is a fuzzy one,” he says. “Call them whatever you want, I don’t care. What is important is that people realize there is hidden diversity.”
My comment: The editors at “Nature” seem to typically support the misrepresentations of the title: new Galapagos tortoise species, despite accurate claims that “The species concept is a fuzzy one.”
Let’s compare what we see this week in “Nature” to what we see in “Science.”
Is the nature of “Nature” pseudoscience? Is “Systems biology” what’s important to “Science?”
Models are simplified (but not simplistic) representations of real systems, and this is precisely the property that makes them attractive to explore the consequences of our assumptions, and to identify where we lack understanding of the principles governing a biological system.
My comment: (published to the “Science” site)
Is anything less than this atoms to ecosystems approach to modeling biologically-based cause and effect going to be acceptable from this point forward?
What this article suggests to me is that others must develop models based on nutrient-energy dependent base pair changes, or that their models cannot be validated with experimental evidence.
Structural diversity of supercoiled DNA
Re: “comparisons of supercoiling-dependent twisted, writhed, curved, and kinked conformations and associated base exposure. Each of these structural features may be differentially recognized by the proteins, nucleic acids, and small molecules that modulate DNA metabolic processes.”
Summary: Claims that mutations in mitochondrial genes led to the biodiversity manifested in Galapagos tortoise species, or any other species should be evaluated in the context of this question: “Is there a model for that?”
If no model of biologically-based cause and effect links mutations in mitochondrial genes to RNA-mediated gene duplication and RNA-mediated amino acid substitutions, the mutations cannot be placed into the context of anything known about nutrient-dependent RNA-mediated cell type differentiation in species from microbes to man, which is controlled by the physiology of reproduction.
Also, ask yourself, would a serious scientist who understands RNA-mediated gene silencing or any other aspect of RNA-mediated epigenetic regulation of gene expression claim that mutations in mitochondrial genes led to anything except pathology?