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大肠杆菌K-12细胞周期的控制机制由环腺苷酸-环腺苷酸受体蛋白复合物触发。

Control mechanism of the Escherichia coli K-12 cell cycle is triggered by the cyclic AMP-cyclic AMP receptor protein complex.

作者信息

Utsumi R, Noda M, Kawamukai M, Komano T

机构信息

Department of Agricultural Chemistry, Kinki University, Higashiosaka, Japan.

出版信息

J Bacteriol. 1989 May;171(5):2909-12. doi: 10.1128/jb.171.5.2909-2912.1989.

Abstract

The role of cyclic AMP (cAMP) in the cell cycle of Escherichia coli K-12 was studied in three mutant strains. One was KI1812, in which the cya promoter is replaced by the lacUV5 promoter. In KI1812, isopropyl-beta-D-thiogalactopyranoside induced the synthesis of cya mRNA, and at the same time cell division was inhibited and short filaments containing multiple nuclei were formed. The other strains were constructed as double mutants (NC6707 cya sulB [ftsZ(Ts)] and TR3318 crp sulB [ftsZ(Ts)]). In both double mutants, filamentation was repressed at 42 degrees C, but it was induced again by addition of cAMP in strain NC6707 and introduction of pHA7 containing wild-type crp in TR3318. These results indicate that lateral wall synthesis in the E. coli cell cycle is triggered by the cAMP-cAMP receptor protein complex.

摘要

在三种突变菌株中研究了环磷酸腺苷(cAMP)在大肠杆菌K-12细胞周期中的作用。一种是KI1812,其中cya启动子被lacUV5启动子取代。在KI1812中,异丙基-β-D-硫代半乳糖苷诱导cya mRNA的合成,同时细胞分裂受到抑制并形成含有多个细胞核的短丝。其他菌株构建为双突变体(NC6707 cya sulB [ftsZ(Ts)]和TR3318 crp sulB [ftsZ(Ts)])。在这两种双突变体中,丝状化在42℃时受到抑制,但在NC6707菌株中通过添加cAMP以及在TR3318中引入含有野生型crp的pHA7再次诱导丝状化。这些结果表明,大肠杆菌细胞周期中的侧壁合成由cAMP - cAMP受体蛋白复合物触发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c27/209987/40a59c2c0f64/jbacter00171-0660-a.jpg

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