In the context of vertebrate wide mutations, mutation-driven evolution is extended across species in this research journal article and in this report about it:
Single nucleotide polymorphism in the neuroplastin locus associates with cortical thickness and intellectual ability in adolescents
Journal article excerpt: “NPTN and other genes involved in neurite outgrowth have recently been identified as direct targets of FOXP2, a transcription factor that when mutated causes a monogenic speech and language disorder in humans and the reduced dosage of which impairs synaptic plasticity, motor-skill learning and ultrasonic vocalizations in mice, and disrupts vocal learning in songbirds. In agreement with our data, this suggests that similar to FOXP2, NPTN may be involved in learning vocal and nonvocal skills. Furthermore, functional polymorphisms in the NPTN promoter that may confer susceptibility to schizophrenia have been identified.”
My comment: Natural selection is removed from consideration in a forthcoming Discover magazine interview article about the author of the book and concept of Mutation-Driven Evolution.
Two questions remain unanswered:
1) What causes mutations that cause monogenic disorders.
2) How does mutation-driven evolution occur without natural selection?
Now that researchers have extended the concept of mutation-driven evolution across species and tentatively linked specific mutations to a monogenic human disorder of development, they must also ready themselves for questions like this: How are vertebrate-wide mutations that alter similar traits such as ultrasonic vocalizations, singing in birds, and human language development transferred from one species to another with or without the involvement of natural selection?
1) Mutant enzymes challenge all assumptions: “Mutant proteins… never have been activated in the first place, and residues that we presumed were important actually play roles quite unlike what we anticipated.”
2) Ecology in the genomics era of a degraded planet: “Our planet’s biological legacy—including all the different habitats on Earth and all the different species that live in them—is the result of eons of natural selection.”
For comparison to the what appears to be collectively unequivocal and repeated refutations of mutation-initiated natural selection in the context of mutation-driven evolution, see:
This model details how chemical ecology drives adaptive evolution via: (1) ecological niche construction, (2) social niche construction, (3) neurogenic niche construction, and (4) socio-cognitive niche construction. This model exemplifies the epigenetic effects of olfactory/pheromonal conditioning, which alters genetically predisposed, nutrient-dependent, hormone-driven mammalian behavior and choices for pheromones that control reproduction via their effects on luteinizing hormone (LH) and systems biology.
But remember the statement that follows, and please do whatever you can to “Save Your Children” from being forced to accept the decades-old ridiculous theories that were taught to their professors who never asked: Is there a model for that?”
Jay R. Feierman: I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.