Natural Selection for olfactory receptor genes
- A correspondent wrote:
Very important article. See last sentence herein.JK: Agreed. I've attempted (with no success) to discuss it in the context of Natural Selection for olfactory receptor genes that in Drosophila are clearly epigenetically linked to experience-dependent monoallelic receptor expression in mammals and to a human odorant receptor, OR7D4, which is selectively activated in vitro by androstenone and the related odorous steroid androstadienone. The moderator of the human ethology yahoo group blocks my posts with claims that they are redundant, and postings to evolutionary psychology or other newsgroups elicit no response -- except 'inspired' side discussions of ridiculous theories.
It may be that you and I are the only two people in the world who are capable of integrating information from across disciplines to result in explanation of cause and effect across species. Others seem to be content with their theories and probably don't want to consider biological facts. I'd probably feel the same way if I hadn't learned anything new in the past 50 years, and was suddenly faced with an article that explained GlobalEpigenomic Reconfiguration During Mammalian Brain Development via the basic principle of biology and levels of biological organization required for adaptive evololution in species from microbes to man.
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"In addition, methylation in the non-CG context (mCH, where H = A, C, or T) is also present in the adult mouse and human brains (20, 21), but is rare or absent in other differentiated cell types (22, 23)." (1)
1. GlobalEpigenomic Reconfiguration During Mammalian Brain Development.
Lister R, Mukamel EA, Nery JR, Urich M, Puddifoot CA, Johnson ND, Lucero J, Huang Y, Dwork AJ, Schultz MD, Yu M, Tonti-Filippini J, Heyn H, Hu S, Wu JC, Rao A, Esteller M, He C, Haghighi FG, Sejnowski TJ, Behrens MM, Ecker JR.
Science. 2013 Jul 4.
Dynamic epigenetic changes have been observed during brain development, maturation and learning (1–6). DNA methylation (mC) is a stable covalent modification that persists in post-mitotic cells throughout their lifetime, defining their cellular identity. However, the methylation status at each of the ~1 billion cytosines in the genome is potentially an information-rich and flexible substrate for epigenetic modification that can be altered by cellular activity (7, 8). Changes in DNA methylation were implicated in learning and memory (9, 10), as well as in age-related cognitive decline (11). Mice with a postnatal deletion of DNA methyl-transferases Dnmt1 and Dnmt3a in forebrain excitatory neurons, or with a global deletion of Methyl-CpG-Binding Protein 2 (MeCP2), show abnormal long-term neural plasticity and cognitive deficits (2, 12).
DNA methylation composition and dynamics in the mammalian brain are highly distinct. 5-hydroxymethylcytosine (hmC), a modification of mC catalyzed by the Tet family of mC hydroxylase proteins, accumulates in the adult brain (13–15) along with its more highly oxidised derivatives 5-formylcytosine and 5-carboxylcytosine. These modifications of mC were implicated as intermediates in an active DNA demethylation pathway (16–19). In addition, methylation in the non-CG context (mCH, where H = A, C, or T) is also present in the adult mouse and human brains (20, 21), but is rare or absent in other differentiated cell types (22, 23). Little is known about cell type-specific patterning of DNA methylation and its dynamics during mammalian brain development. Here we provide integrated empirical data and analysis of DNA methylation at single base resolution, across entire genomes, with cell-type and developmental specificity. These results extend our knowledge of the unique role of DNA methylation in brain development and function, and offer a new framework for testing the role of the epigenome in healthy function and in pathological disruptions of neural circuits....
Supporting previous studies, we found that mammalian brain mCH is typically depleted in expressed genes, with genic mCH level inversely proportional to the abundance of the associated transcript (Fig. 1 A, B) (20). This pattern is the opposite of that observed in embryonic stem (ES) cells (22) and suggests that genic mCH in the brain may inhibit transcription. The absence of mCH in fetal brain suggests that this signature for gene repression is added to the genome at a later developmental stage....
Genome-wide detection of hmC by cytosine 5-methylenesulphonate immunoprecipitation (CMS-IP) (38, 39) revealed that hmC is also strongly depleted in the VH locus. mCH-deserts are observed at other loci in the genome, including olfactory receptor gene clusters that form heterochromatic aggregates required for monoallelic receptor expression in olfactory sensory neurons (40, 41).--
James V. Kohl
Medical laboratory scientist (ASCP)
Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlledadaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.
These two published works are based on accurate representations of the conserved molecular mechanisms first detailed in the context of molecular epigenetics in our 1996 Hormones and Behavior review article:FromFertilization to Adult Sexual Behavior
See also: 2001 Human pheromones: integrating neuroendocrinology and ethology
2006/7 The Mind's Eyes: Human pheromones, neuroscience, and male sexual preferences