A DNA damage checkpoint in Caulobacter crescentus inhibits cell division through a direct interaction with FtsW.
نویسندگان
چکیده
Following DNA damage, cells typically delay cell cycle progression and inhibit cell division until their chromosomes have been repaired. The bacterial checkpoint systems responsible for these DNA damage responses are incompletely understood. Here, we show that Caulobacter crescentus responds to DNA damage by coordinately inducing an SOS regulon and inhibiting the master regulator CtrA. Included in the SOS regulon is sidA (SOS-induced inhibitor of cell division A), a membrane protein of only 29 amino acids that helps to delay cell division following DNA damage, but is dispensable in undamaged cells. SidA is sufficient, when overproduced, to block cell division. However, unlike many other regulators of bacterial cell division, SidA does not directly disrupt the assembly or stability of the cytokinetic ring protein FtsZ, nor does it affect the recruitment of other components of the cell division machinery. Instead, we provide evidence that SidA inhibits division by binding directly to FtsW to prevent the final constriction of the cytokinetic ring.
منابع مشابه
A DNA Damage-Induced, SOS-Independent Checkpoint Regulates Cell Division in Caulobacter crescentus
Cells must coordinate DNA replication with cell division, especially during episodes of DNA damage. The paradigm for cell division control following DNA damage in bacteria involves the SOS response where cleavage of the transcriptional repressor LexA induces a division inhibitor. However, in Caulobacter crescentus, cells lacking the primary SOS-regulated inhibitor, sidA, can often still delay d...
متن کاملRegulatory pathways controlling cell division after DNA damage in
All cells must coordinate DNA replication with cell division in order to faithfully propagate whole chromosomes to daughter cells. During episodes of DNA damage, cells often delay division until the lesions have been repaired and replication has completed. The paradigm for the bacterial response to DNA damage is the transcriptional induction of "SOS" genes, and many organisms encode an SOS-indu...
متن کاملNo SOS Needed: A Second Bacterial Checkpoint System Stops Cell Division
Cell division must be tightly coordinated with DNA replication so that a complete genome ends up in each daughter cell. That coordination is especially critical when DNA is damaged, as lengthy delays may be required to repair broken strands. To prevent premature division, cells detect the presence of broken DNA with dedicated sensor proteins, which inhibit division while they promote repair. In...
متن کاملPap1+ confers microtubule damage resistance to mut2a, an extragenic suppressor of the rad26:4A allele in S. pombe.
The DNA structure checkpoint protein Rad26ATRIP is also required for an interphase microtubule damage response. This checkpoint delays spindle pole body separation and entry into mitosis following treatment of cells with microtubule poisons. This checkpoint requires cytoplasmic Rad26ATRIP, which is compromised by the rad26:4A allele that inhibits cytoplasmic accum...
متن کاملCoordination between chromosome replication, segregation, and cell division in Caulobacter crescentus.
Progression through the Caulobacter crescentus cell cycle is coupled to a cellular differentiation program. The swarmer cell is replicationally quiescent, and DNA replication initiates at the swarmer-to-stalked cell transition. There is a very short delay between initiation of DNA replication and movement of one of the newly replicated origins to the opposite pole of the cell, indicating the ab...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Genes & development
دوره 25 12 شماره
صفحات -
تاریخ انتشار 2011