Lack of S-adenosylmethionine results in a cell division defect in Escherichia coli.

نویسندگان

  • E B Newman
  • L I Budman
  • E C Chan
  • R C Greene
  • R T Lin
  • C L Woldringh
  • R D'Ari
چکیده

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.

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عنوان ژورنال:
  • Journal of bacteriology

دوره 180 14  شماره 

صفحات  -

تاریخ انتشار 1998