IDENTIFICATION OF A NOVEL RESPONSE REGULATOR REQUIRED FOR THE SWARMER-TO-STALKED-CELL TRANSITION IN CAULOBACTER-CRESCENTUS
IDENTIFICATION OF A NOVEL RESPONSE REGULATOR REQUIRED FOR THE SWARMER-TO-STALKED-CELL TRANSITION IN CAULOBACTER-CRESCENTUS
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DOI：
10.1128/jb.177.21.6223-6229.1995
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发表时间：
1995-11-01
影响因子：
3.2
通讯作者：
NEWTON, A
中科院分区：
文献类型：
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作者：
HECHT, GB;NEWTON, A
新月柄杆菌细胞周期后期运动的开始取决于组氨酸激酶 PleC 和反应调节因子 DivK 介导的信号转导途径。我们现在表明，pleD 的功能是运动群细胞随后失去运动和茎形成所必需的，它编码具有串联 N 端反应调节域 D1 和 D2 的 454 个残基蛋白，以及一个新颖的 C 端 GGDEF 结构域。 pleD301（pleC Mot 表型的半显性抑制因子）的鉴定被认为是一种突变，预计会导致 D1 结构域中的 D-53-->G 变化，这支持了 PleD 调节因子中磷酸化的作用。在 pleD 开放阅读框中构建的破坏表明该基因不是必需的，并且 pleC 表型也可以通过隐性、功能丧失突变来抑制。这些结果表明，PleD 是控制 C. crescentus 细胞周期早期有柄细胞分化的信号转导途径的一部分。
The onset of motility late in the Caulobacter crescentus cell cycle depends on a signal transduction pathway mediated by the histidine kinase PleC and response regulator DivK We now show that pleD, whose function is required for the subsequent loss of motility and stalk formation by the motile swarmer cell, encodes a 454-residue protein with tandem N-terminal response regulator domains D1 and D2 and a novel C-terminal GGDEF domain. The identification of pleD301, a semidominant suppressor of the pleC Mot phenotype, as a mutation predicted to result in a D-53-->G change in the D1 domain supports a role for phosphorylation in the PleD regulator. Disruptions constructed in the pleD open reading frame demonstrated that the gene is not essential and that the pleC phenotype can also be suppressed by a recessive, loss-of-function mutation. These results suggest that PleD is part of a signal transduction pathway controlling stalked-cell differentiation early in the C. crescentus cell cycle.