Regulated proteolysis of a transcription factor complex is critical to cell cycle progression in Caulobacter crescentus
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Laub_Regulated proteolysis.pdf
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Author(s)
Gora, Kasia G.
Cantin, Amber
Joshi, Kamal K.
Wohlever, Matthew Lee
Perchuk, Barrett
Chien, Peter, 1976-
Laub, Michael T
Date Issued
February 2013
Journal
Molecular Microbiology
Publisher
Wiley Blackwell
Citation
Gora, Kasia G., Amber Cantin, Matthew Wohlever, Kamal K. Joshi, Barrett S. Perchuk, Peter Chien, and Michael T. Laub. “Regulated proteolysis of a transcription factor complex is critical to cell cycle progression in Caulobacter crescentus.” Molecular Microbiology 87, no. 6 (March 25, 2013): 1277-1289.
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Author's final manuscript
Abstract
Cell cycle transitions are often triggered by the proteolysis of key regulatory proteins. In Caulobacter crescentus, the G1-S transition involves the degradation of an essential DNA-binding response regulator, CtrA, by the ClpXP protease. Here, we show that another critical cell cycle regulator, SciP, is also degraded during the G1-S transition, but by the Lon protease. SciP is a small protein that binds directly to CtrA and prevents it from activating target genes during G1. We demonstrate that SciP must be degraded during the G1-S transition so that cells can properly activate CtrA-dependent genes following DNA replication initiation and the reaccumulation of CtrA. These results indicate that like CtrA, SciP levels are tightly regulated during the Caulobacter cell cycle. In addition, we show that formation of a complex between CtrA and SciP at target promoters protects both proteins from their respective proteases. Degradation of either protein thus helps trigger the destruction of the other, facilitating a cooperative disassembly of the complex. Collectively, our results indicate that ClpXP and Lon each degrade an important cell cycle regulator, helping to trigger the onset of S phase and prepare cells for the subsequent programmes of gene expression critical to polar morphogenesis and cell division.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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DOI of Published Version
https://doi.org/10.1111/mmi.12166
