Journal
MOLECULAR MICROBIOLOGY
Volume 70, Issue 3, Pages 608-622Publisher
WILEY
DOI: 10.1111/j.1365-2958.2008.06423.x
Keywords
-
Categories
Funding
- Nara Institute of Science and Technology (NAIST)
- Scientific Research on Priority Areas [17013060]
- Academic Frontier Project for Private Universities at Kinki University [17370063]
- Global COE Program
- NAIST from MEXT, Japan
- Grants-in-Aid for Scientific Research [17013060, 17370063] Funding Source: KAKEN
Ask authors/readers for more resources
Escherichia coli dinB encodes the specialized DNA polymerase DinB (Pol IV), which is induced as part of the SOS stress-response system and functions in translesion synthesis (TLS) to relieve the replicative Pol III that is stalled at DNA lesions. As the number of DinB molecules, even in unstressed cells, is greater than that required to accomplish TLS, it is thought that dinB plays some additional physiological role. Here, we overexpressed dinB under the tightly regulable arabinose promoter and looked for a distinct phenotype. Upon induction of dinB expression, progression of the replication fork was immediately inhibited at random genomic positions, and the colony-forming ability of the cells was reduced. Overexpression of mutated dinB alleles revealed that the structural requirements for these two inhibitory effects and for TLS were distinct. The extent of in vivo inhibition displayed by a mutant DinB matched the extent of its in vitro impedance, at near-physiological concentration, of a moving Pol III. We suggest that DinB targets Pol III, thereby acting as a brake on replication fork progression. Because the brake operates when cells have excess DinB, as they do under stress conditions, it may serve as a checkpoint that modulates replication to safeguard genome stability.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available