Subscription required: The logic of gene regulatory networks in early vertebrate forebrain patterning Review Article Mechanisms of Development, Available online 27 October 2012 Leonardo Beccari, Raquel Marco-Ferreres, Paola Bovolenta
Excerpt: “This molecular picture of how the forebrain forms will also hopefully help to decipher the causes of the many still poorly understood pathologies linked to alterations in forebrain development. These include for example autism or schizophrenia and congenital defects of the eye such as anophthalmia or microphthalmia.”
My comment: This review represents a very technical but cohesive and comprehensive approach to what can only be nutrient chemical-dependent and pheromone-controlled vertebrate brain development. Briefly portrayed is the role of loss-of-function mutations that result in hypothalamic defects, which have little impact on other forebrain structures.
For contrast, Work by Wagner & Lynch (2008) is referenced that takes us forward to their 2011 report (with others), which suggests 1532 genes were recruited into endometrial expression during the evolution of pregnancy in placental mammals. These authors are among others who have questioned whether the origin of new cell types, which involves the recruitment of hundreds of genes, can be achieved via random mutations and small-scale changes. It is more likely that nutrient chemicals and pheromones cause the epigenetic tweaking of immense gene networks in superorganisms that solve problems through the exchange and the selective cancellation and modification of signals. This epigenetic tweaking (aka biological embedding in the context of adaptive evolution) best represents what appears to be a systematic force instead of a mutational bias. The systematic force is associated with a specific origination mechanism that contributes to an excess of young genes in the fetal brain.
This correct representation of this systematic force shows that loss-of-function mutations are less important to individual survival and species survival in mammals when compared to the obvious role of nutrient chemical-dependent, microRNA-driven, epigenetic effects on intracellular signaling and stochastic gene expression. These epigenetic effects of nutrient chemicals are controlled by the epigenetic effects of pheromones on the same gene regulatory networks via messenger RNA and intermolecular changes in gene expression that lead to adaptive evolution across species from microbes to man (e.g., in my model).
What is most pertinent in the context of my model for adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction is the relative insignificance of congenital defects of the eye in the context of developmental disorders like autism and schizophrenia. When compared to congenital defects that result from perturbed migration of gonadotropin releasing hormone (GnRH) neurosecretory neurons into the brain during embryonic development, there is no other adaptively evolved in utero development of a neurogenic niche (aka a specific group of cells known as “organizing centres” like the hypothalamic GnRH neuronal niche) that links the sensory environment directly to secretion of the hormone: GnRH, which is the primary modulator of brain development in vertebrate species.
Adaptively evolved vertebrate GnRH secretion results from the conservation of similar molecules from microbes (e.g., yeasts) to man, and diversification of its receptor (GnRHR) across 400 million years of vertebrate evolution. The reciprocal relationships between other neuronal systems linked to vertebrate behavioral development via their interactions with GnRH and various aspects of GnRH-controlled hormone-receptor content in diverse brain tissues of mammals may help to return focus on behavioral development to inclusion of its biological underpinnings in brain development.
As an alternative, we could continue to approach disorders of behavioral development from individual perspectives on how hormones like dopamine, oxytocin, norepinephrine, testosterone, estrogens et al. affect behavior without first linking them either to the sensory, or to the social environment of any species as if nothing were known about epigenetic links between nature and nurture. Clearly, however, we should dispense with theory and statistical analyses that do not address these epigenetic links between nature and nurture.
