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Cell cycle‐dependent abundance, stability and localization of FtsA and FtsQ in Caulobacter crescentus
Author(s) -
Martin Miriam E.,
Trimble Michael J.,
Brun Yves V.
Publication year - 2004
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2004.04251.x
Subject(s) - caulobacter crescentus , cell division , biology , cell cycle , ftsz , microbiology and biotechnology , cell growth , dna replication , cell , cell cycle protein , genetics , dna
Summary Coordination between cell division and DNA replication is ensured by checkpoints that act through proteins required for cell division. Following a block in DNA replication, transcription of the cell division progression genes ftsA and ftsQ is prevented in Caulobacter crescentus . One requirement for this checkpoint is that FtsA and/or FtsQ should be limiting for division in the next cell cycle. We show that the number of FtsA and FtsQ molecules fluctuates such that their concentration is low in swarmer and stalked cells, peaks in pre‐divisional cells, and then dramatically decreases after cell division. Despite constitutive expression from an inducible promoter, FtsA and FtsQ levels still vary during the cell cycle, and the half‐life of FtsA increases from 13 min in swarmer cells to 55 min in stalked cell types, confirming cell type‐specific degradation. The post‐division degradation of FtsA and FtsQ in swarmer cells reduces their concentration to 7% and 10% of their maximal level, respectively, strongly suggesting that de novo synthesis of both proteins is required for each division cycle. The localization of FtsA and FtsQ is also cell type‐specific. FtsA and FtsQ are recruited to the midcell during a short period in late pre‐divisional cells, consistent with the demonstrated requirement of FtsA for late stages of cell division. As previously reported for FtsZ, constitutive expression of FtsA causes cell division defects. These results indicate that the tight control of FtsA, and probably FtsQ, by cell cycle transcription, proteolysis, and localization are critical for optimal cell division and the coordination of cell division with the DNA replication cycle.