Derivation of a basic mechanism of control for embryonic genes as a specific subset.
The alpha-fetoprotein gene is conceived as being methylated in the zygote and according to the model is in a heterochromatic state and is therefore in a non-functional condition. Specific DNA methylase genes would produce methylases capable of alkylating enhancer regions of alpha-fetoprotein and certain proteins that would alter the heterochromatin condition. Also involved is a gene for the synthesis of a conformational-inducer protein that is proposed to be capable of blocking genic regions from reheterochromatizing. One of the pivotal events is the accumulation of S-adenosyl-L-methionine that reaches intracellular pool concentrations allowing other redundant active S-adenosyltransferase genes to become active. During embryogenesis specific conformational-inducer proteins would block genes such as the gene for albumin from reheterochromatizing while alpha-fetoprotein gene becomes heterochromatized during subsequent cell cycles. This heterochromatin is formed with embryonic type proteins sensitive to ribosylation-induced conformational changes. The increase in synthesis of alpha-fetoprotein followed by a decrease as albumin synthesis increases during embryogenesis is predicted by the scheme.
D000818:Animals; D005314:Embryonic and Fetal Development / Q000235:genetics*; D004742:Enhancer Elements, Genetic; D008099:Liver / Q000196:embryology; D008938:Mitosis; D008957:Models, Genetic; D009690:Nucleic Acid Conformation; D000509:alpha-Fetoproteins / Q000235:genetics
D000509:alpha-Fetoproteins