This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Centore, R. C.
Right arrow Articles by Sandler, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Centore, R. C.
Right arrow Articles by Sandler, S. J.

 Previous Article  |  Next Article 

Journal of Bacteriology, March 2009, p. 1429-1438, Vol. 191, No. 5
0021-9193/09/$08.00+0     doi:10.1128/JB.01415-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

UvrD303, a Hyperhelicase Mutant That Antagonizes RecA-Dependent SOS Expression by a Mechanism That Depends on Its C Terminus{triangledown} ,{dagger}

Richard C. Centore,1 Michael C. Leeson,2 and Steven J. Sandler1,2*

Molecular and Cellular Biology Graduate Program, Morrill Science Center,1 Department of Microbiology, Morrill Science Center IV N203, University of Massachusetts at Amherst, Amherst, Massachusetts 010032

Received 8 October 2008/ Accepted 4 December 2008

Genomic integrity is critical for an organism's survival and ability to reproduce. In Escherichia coli, the UvrD helicase has roles in nucleotide excision repair and methyl-directed mismatch repair and can limit reactions by RecA under certain circumstances. UvrD303 (D403A D404A) is a hyperhelicase mutant, and when expressed from a multicopy plasmid, it results in UV sensitivity (UVs), recombination deficiency, and antimutability. In order to understand the molecular mechanism underlying the UVs phenotype of uvrD303 cells, this mutation was transferred to the E. coli chromosome and studied in single copy. It is shown here that uvrD303 mutants are UV sensitive, recombination deficient, and antimutable and additionally have a moderate defect in inducing the SOS response after UV treatment. The UV-sensitive phenotype is epistatic with recA and additive with uvrA and is partially suppressed by removing the LexA repressor. Furthermore, uvrD303 is able to inhibit constitutive SOS expression caused by the recA730 mutation. The ability of UvrD303 to antagonize SOS expression was dependent on its 40 C-terminal amino acids. It is proposed that UvrD303, via its C terminus, can decrease the levels of RecA activity in the cell.


* Corresponding author. Mailing address: Department of Microbiology, Morrill Science Center IV N203, University of Massachusetts at Amherst, Amherst, MA 01003. Phone: (413) 577-4391. Fax: (413) 545-1578. E-mail: sandler{at}microbio.umass.edu

{triangledown} Published ahead of print on 12 December 2008.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.


Journal of Bacteriology, March 2009, p. 1429-1438, Vol. 191, No. 5
0021-9193/09/$08.00+0     doi:10.1128/JB.01415-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Murphy, M. N., Gong, P., Ralto, K., Manelyte, L., Savery, N. J., Theis, K. (2009). An N-terminal clamp restrains the motor domains of the bacterial transcription-repair coupling factor Mfd. Nucleic Acids Res 37: 6042-6053 [Abstract] [Full Text]