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

被引:52
作者
Newman, EB
Budman, LI
Chan, EC
Greene, RC
Lin, RT
Woldringh, CL
D'Ari, R
机构
[1] Concordia Univ, Dept Biol, Montreal, PQ H3G 1M8, Canada
[2] McGill Univ, Fac Med, Dept Microbiol, Montreal, PQ H3A 2B4, Canada
[3] Sir Mortimer B Davis Jewish Hosp, Lady Davis Inst Med Res, Montreal, PQ H3T 1E2, Canada
[4] Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA
[5] US Vet Adm Med Ctr, Durham, NC 27710 USA
[6] Univ Amsterdam, BioCentrum, Sect Mol Cytol, Inst Mol Cell Biol, NL-1098 SM Amsterdam, Netherlands
[7] Univ Paris 07, CNRS, Inst Jacques Monod, F-75251 Paris 05, France
[8] Univ Paris 06, CNRS, Inst Jacques Monod, F-75251 Paris 05, France
关键词
D O I
10.1128/JB.180.14.3614-3619.1998
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:3614 / 3619
页数:6
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