Genetic adaptation controlled by methylations and acetylations at the nuclear and cytosolic levels: a hypothetical model.

Metabolic sensors related to the maturation of metabolism seem to control a process of generic adaptation involving the silencing of genes and the expression of their copies more adapted to environmental changes. Nuclear methylases and histone deacetylases control the gene silencing process. Nuclear methylases compete with cytosolic methylases for the same methyl donnors, this will favor the expression of unmethylated more adapted gene copies, when cytosotic methylases take over. Methylated cytosolic compounds may then represent an index of this adaptation. If a more adapted gene copy is mutated, the regulatory ligand of the gene product that does not find its target may induce a reexpression of the silenced gene. The hypothetical model proposed considers that gene silencing and expression of a more adequate copy involves a non-specific gene silencer switch that depends on the histone status; the silencer switch is counteracted by the ligand of the adapted gene copy product acting like an inducer.