A Cell-Type-Specific Protein-Protein Interaction Modulates Transcriptional Activity of a Master Regulator in Caulobacter crescentus

被引:71
作者
Gora, Kasia G. [1 ]
Tsokos, Christos G. [1 ]
Chen, Y. Erin [1 ]
Srinivasan, Balaji S. [3 ,4 ]
Perchuk, Barrett S. [1 ,2 ]
Laub, Michael T. [1 ,2 ]
机构
[1] MIT, Dept Biol, Cambridge, MA 02139 USA
[2] MIT, Howard Hughes Med Inst, Cambridge, MA 02139 USA
[3] Stanford Univ, Dept Comp Sci, Stanford, CA 94305 USA
[4] Stanford Univ, Dept Stat, Stanford, CA 94305 USA
基金
美国国家卫生研究院;
关键词
RESPONSE REGULATOR; CYCLE PROGRESSION; HISTIDINE KINASE; BINDING-SITES; PHOSPHORYLATION; IDENTIFICATION; LOCALIZATION; REPLICATION; EXPRESSION; INHIBITOR;
D O I
10.1016/j.molcel.2010.06.024
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Progression through the Caulobacter cell cycle is driven by the master regulator CtrA, an essential two-component signaling protein that regulates the expression of nearly 100 genes. CtrA is abundant throughout the cell cycle except immediately prior to DNA replication. However, the expression of CtrA-activated genes is generally restricted to S phase. We identify the conserved protein SciP (small CtrA inhibitory protein) and show that it accumulates during G1, where it inhibits CtrA from activating target genes. The depletion of SciP from G1 cells leads to the inappropriate induction of CtrA-activated genes and, consequently, a disruption of the cell cycle. Conversely, the ectopic synthesis of SciP is sufficient to inhibit CtrA-dependent transcription, also disrupting the cell cycle. SciP binds directly to CtrA without affecting stability or phosphorylation; instead, SciP likely prevents CtrA from recruiting RNA polymerase. CtrA is thus tightly regulated by a protein-protein interaction which is critical to cell-cycle progression.
引用
收藏
页码:455 / 467
页数:13
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