Epigenetic Principles of Evolution (Elsevier Insights)
Nelson R. Cabej
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This is the first and only book, so far, to deal with the causal basis of evolution from an epigenetic view. By revealing the epigenetic "user" of the "genetic toolkit", this book demonstrates the primacy of epigenetic mechanisms and epigenetic information in generating evolutionary novelties.
The author convincingly supports his theory with a host of examples from the most varied fields of biology, by emphasizing changes in developmental pathways as the basic source of evolutionary change in metazoans.
- Original and thought provoking--a radically new theory that overcomes the present difficulties of the theory of evolution
- Is the first and only theory that uses epigenetic mechanisms and principles for explaining evolution of metazoans
- Takes an integrative approach and shows a wide range of learning
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of the ICS, with the CNS as its controller. The term “homeostasis” here will be used in a broader sense to comprise not only the maintenance of the steady state of the body fluids but also the maintenance of the normal structure and function of the animal organism in its entirety. Modern physiology provides ample evidence on the CNS control of vital functions of all the organs and organ systems in animals, including heart work, blood circulation and pressure, respiration, digestion, and endocrine
Determination of Phenotypic Traits in Metazoans 19 PFC OB PAG LS NAcc AVP OT VP PVN MeA VTA NTS DA Figure 1.7 Proposed neural circuitry of social bonding in monogamous prairie voles. Somatosensory input from the penis or vagina impinge on the nucleus tractus solitarius (NTS) and midbrain periaqueductal gray (PAG), which then project to the nucleus accumbens (NAcc) and paraventricular nucleus (PVN). Olfactory information is conveyed via the olfactory bulb to the medial amygdala (MeA),
the greater the effect of the change could be. So the first conclusion to be drawn is that no single gene is responsible for the formation of the affected character. To single out a particular gene as the cause of the phenotypic character in such cases is to attribute to the part the functions of the whole. The fact that the signal cascades that activate GRNs start with electrical/chemical outputs of the processing of internal/external signals in neural circuits suggests that the
excess RA causes phagocytosis of the migrating neural crest cells, leading to craniofacial malformations (Yasuda et al., 1989). In some species, RA is present as maternal factor in the egg cytoplasm, and during the early gastrulation in mammals the main site of RA synthesis may be the mesoderm adjacent to the node and primitive streak (Niederreither et al., 1997). Later in the mouse embryogenesis (E11), RA is produced in an endocrine way in the incipient adrenal gland. RA penetrates cell membrane