A cell-type-specific protein-protein interaction modulates transcriptional activity of a master regulator in Caulobacter crescentus.
A cell-type-specific protein-protein interaction modulates transcriptional activity of a master regulator in Caulobacter crescentus.
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DOI：
10.1016/j.molcel.2010.06.024
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发表时间：
2010-08-13
期刊：
影响因子：
16
通讯作者：
Laub MT
中科院分区：
文献类型：
--
作者：
Gora KG;Tsokos CG;Chen YE;Srinivasan BS;Perchuk BS;Laub MT
通过柄杆菌细胞周期的进展是由主调节因子CtrA驱动的，CtrA是一种调节近100个基因表达的必需的双组分信号蛋白。CtrA在整个细胞周期中是丰富的，除了紧接在DNA复制之前。然而，CtrA激活基因的表达通常限于S期。我们鉴定了保守蛋白SciP（小CtrA抑制蛋白），并表明它在G1期间积累，在G1期间它抑制CtrA激活靶基因。SciP从G1细胞中的消耗导致CtrA激活基因的不适当诱导，从而导致细胞周期的破坏。相反，SciP的异位合成足以抑制CtrA依赖性转录，也破坏细胞周期。SciP直接与CtrA结合而不影响稳定性或磷酸化;相反，SciP可能会阻止CtrA招募RNA聚合酶。因此，CtrA受到蛋白质-蛋白质相互作用的严格调控，这对细胞周期进程至关重要。
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.
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影响因子：
64.5
作者：
Domian, IJ;Quon, KC;Shapiro, L
通讯作者：
Shapiro, L
影响因子：
3.6
作者：
Dutton, RJ;Xu, ZH;Gober, JW
通讯作者：
Gober, JW
DOI：
10.1073/pnas.0637648100
发表时间：
2003-04-01
影响因子：
11.1
作者：
Nakano, S;Nakano, MM;Zuber, P
通讯作者：
Zuber, P
影响因子：
64.5
作者：
McGrath, PT;Iniesta, AA;McAdams, HH
通讯作者：
McAdams, HH
影响因子：
11.4
作者：
Jenal, U;Fuchs, T
通讯作者：
Fuchs, T