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柄杆菌从S期到G1期的细胞周期转变由祖先毒力调节因子介导。

Cell cycle transition from S-phase to G1 in Caulobacter is mediated by ancestral virulence regulators.

作者信息

Fumeaux Coralie, Radhakrishnan Sunish Kumar, Ardissone Silvia, Théraulaz Laurence, Frandi Antonio, Martins Daniel, Nesper Jutta, Abel Sören, Jenal Urs, Viollier Patrick H

机构信息

Department Microbiology and Molecular Medicine, Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1, 1211 Genève 4, Switzerland.

1] Department Microbiology and Molecular Medicine, Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1, 1211 Genève 4, Switzerland [2].

出版信息

Nat Commun. 2014 Jun 18;5:4081. doi: 10.1038/ncomms5081.

Abstract

Zinc-finger domain transcriptional regulators regulate a myriad of functions in eukaryotes. Interestingly, ancestral versions (MucR) from Alpha-proteobacteria control bacterial virulence/symbiosis. Whether virulence regulators can also control cell cycle transcription is unknown. Here we report that MucR proteins implement a hitherto elusive primordial S→G1 transcriptional switch. After charting G1-specific promoters in the cell cycle model Caulobacter crescentus by comparative ChIP-seq, we use one such promoter as genetic proxy to unearth two MucR paralogs, MucR1/2, as constituents of a quadripartite and homeostatic regulatory module directing the S→G1 transcriptional switch. Surprisingly, MucR orthologues that regulate virulence and symbiosis gene transcription in Brucella, Agrobacterium or Sinorhizobium support this S→G1 switch in Caulobacter. Pan-genomic ChIP-seq analyses in Sinorhizobium and Caulobacter show that this module indeed targets orthologous genes. We propose that MucR proteins and possibly other virulence regulators primarily control bacterial cell cycle (G1-phase) transcription, rendering expression of target (virulence) genes periodic and in tune with the cell cycle.

摘要

锌指结构域转录调节因子调控真核生物中的众多功能。有趣的是,来自α-变形菌的祖先版本(MucR)控制细菌的毒力/共生。毒力调节因子是否也能控制细胞周期转录尚不清楚。在此,我们报告MucR蛋白实现了一种迄今为止难以捉摸的原始S→G1转录开关。通过比较染色质免疫沉淀测序(ChIP-seq)在细胞周期模型新月柄杆菌中绘制G1特异性启动子后,我们使用其中一个这样的启动子作为遗传代理,发掘出两个MucR旁系同源物MucR1/2,它们是指导S→G1转录开关的四方稳态调节模块的组成部分。令人惊讶的是,在布鲁氏菌、根癌土壤杆菌或中华根瘤菌中调节毒力和共生基因转录的MucR直系同源物在新月柄杆菌中支持这种S→G1开关。在中华根瘤菌和新月柄杆菌中的泛基因组ChIP-seq分析表明,该模块确实靶向直系同源基因。我们提出,MucR蛋白以及可能的其他毒力调节因子主要控制细菌细胞周期(G1期)转录,使靶标(毒力)基因的表达具有周期性并与细胞周期同步。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a3e/4083442/b6e6728a1f2c/ncomms5081-f1.jpg

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