Theorectical mechanisms for synthesis of carcinogen-induced embryonic proteins: III. The tRNA methylases; methylation mechanism and function.
It is contended that redundant repressed tRed) with carcinogens in adult cells. Supportive evidence, especially from molecular model building, is presented for a mechanism of tRNA methylation. In this mechanism the adenine moiety of S-adenosyl-L-methionine base-pairs with uracil for all tRNA methylations. Furthermore it is proposed that such methylations are required during the transcription of a tRNA molecule in order to limit the number of possible conformers that can occur before further development of the molecule takes place. This theory of the function for methyl groups is discussed in the light of the properties found for hypomethylated tRNAs.
D000818:Animals; D002273:Carcinogens / Q000494:pharmacology*; D004790:Enzyme Induction; D005326:Fetal Proteins / Q000096:biosynthesis* / Q000235:genetics; D005333:Fetus / Q000378:metabolism; D008099:Liver / Q000201:enzymology; D008745:Methylation; D008958:Models, Molecular; D010641:Phenotype; D010649:Phenylalanine / Q000378:metabolism; D012343:RNA, Transfer / Q000378:metabolism; D051381:Rats; D015003:Yeasts / Q000378:metabolism; D012359:tRNA Methyltransferases / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*
D002273:Carcinogens; D005326:Fetal Proteins; D010649:Phenylalanine; D012343:RNA, Transfer; D012359:tRNA Methyltransferases