Lack of S-Adenosylmethionine Results in a Cell Division Defect in Escherichia coli
AUTOR(ES)
Newman, E. B.
FONTE
American Society for Microbiology
RESUMO
The enzyme S-adenosylmethionine (SAM) synthetase, the Escherichia coli metK gene product, produces SAM, the cell’s major methyl donor. We show here that SAM synthetase activity is induced by leucine and repressed by Lrp, the leucine-responsive regulatory protein. When SAM synthetase activity falls below a certain critical threshold, the cells produce long filaments with regularly distributed nucleoids. Expression of a plasmid-carried metK gene prevents filamentation and restores normal growth to the metK mutant. This indicates that lack of SAM results in a division defect.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=107330Documentos Relacionados
- Regulation of S-Adenosylmethionine Synthetase in Escherichia coli
- Novel Escherichia coli K-12 mutants impaired in S-adenosylmethionine synthesis.
- The effect of methionine and S-adenosylmethionine on S-adenosylmethionine levels in the rat brain
- Lowering S-Adenosylmethionine Levels in Escherichia coli Modulates C-to-T Transition Mutations
- S-Adenosylmethionine Transport in Rickettsia prowazekii