细胞周期的协调和极性定位蛋白对细菌染色体分离动力学的调控。
Cell cycle coordination and regulation of bacterial chromosome segregation dynamics by polarly localized proteins.
机构信息
Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT, USA.
出版信息
EMBO J. 2010 Sep 15;29(18):3068-81. doi: 10.1038/emboj.2010.207. Epub 2010 Aug 27.
Abstract
What regulates chromosome segregation dynamics in bacteria is largely unknown. Here, we show in Caulobacter crescentus that the polarity factor TipN regulates the directional motion and overall translocation speed of the parS/ParB partition complex by interacting with ParA at the new pole. In the absence of TipN, ParA structures can regenerate behind the partition complex, leading to stalls and back-and-forth motions of parS/ParB, reminiscent of plasmid behaviour. This extrinsic regulation of the parS/ParB/ParA system directly affects not only division site selection, but also cell growth. Other mechanisms, including the pole-organizing protein PopZ, compensate for the defect in segregation regulation in ΔtipN cells. Accordingly, synthetic lethality of PopZ and TipN is caused by severe chromosome segregation and cell division defects. Our data suggest a mechanistic framework for adapting a self-organizing oscillator to create motion suitable for chromosome segregation.
摘要
在细菌中，有哪些因素调控着染色体的分离动力学，目前还知之甚少。在这里，我们在新月柄杆菌中发现，极性因子 TipN 通过与新极点的 ParA 相互作用，调节 parS/ParB 分区复合物的定向运动和整体易位速度。在没有 TipN 的情况下，ParA 结构可以在分区复合物后面重新形成，导致 parS/ParB 的停顿和来回运动，类似于质粒的行为。这种对 parS/ParB/ParA 系统的外在调节不仅直接影响到分裂位点的选择，还影响到细胞的生长。其他机制，包括极组织蛋白 PopZ，补偿了 ΔtipN 细胞中分离调控的缺陷。因此，PopZ 和 TipN 的合成致死性是由严重的染色体分离和细胞分裂缺陷引起的。我们的数据为适应自我组织振荡器的机制框架提供了依据，以产生适合染色体分离的运动。
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