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 Google Scholar
Google Scholar
Right arrow Articles by Rajpurohit, Y. S.
Right arrow Articles by Misra, H. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rajpurohit, Y. S.
Right arrow Articles by Misra, H. S.

 Previous Article  |  Next Article 

Journal of Bacteriology, June 2008, p. 3948-3954, Vol. 190, No. 11
0021-9193/08/$08.00+0     doi:10.1128/JB.00026-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Involvement of a Protein Kinase Activity Inducer in DNA Double Strand Break Repair and Radioresistance of Deinococcus radiodurans{triangledown} ,{dagger}

Yogendra S. Rajpurohit,1 Roja Gopalakrishnan,2 and Hari S. Misra1*

Molecular Biology Division,1 Nuclear Agriculture & Biotechnology Division, Bhabha Atomic Research Centre, Mumbai 400 085, India2

Received 7 January 2008/ Accepted 16 March 2008

Transgenic bacteria producing pyrroloquinoline quinone, a known cofactor for dehydrogenases and an inducer of a periplasmic protein kinase activity, show resistance to both oxidative stress and protection from nonoxidative effects of radiation and DNA-damaging agents. Deinococcus radiodurans R1 encodes an active pyrroloquinoline quinone synthase, and constitutive synthesis of pyrroloquinoline quinone occurred in wild-type bacteria. Disruption of a genomic copy of pqqE resulted in cells that lacked this cofactor. The mutant showed a nearly 3-log decrease in {gamma} radiation resistance and a 2-log decrease in mitomycin C tolerance compared to wild-type cells. The mutant cells did not show sensitivity to UVC radiation. Expression of pyrroloquinoline quinone synthase in trans showed that there was functional complementation of {gamma} resistance and mitomycin C tolerance in the pqqE mutant. The sensitivity to {gamma} radiation was due to impairment or slow kinetics of DNA double strand break repair. Low levels of 32P incorporation were observed in total soluble proteins of mutant cells compared to the wild type. The results suggest that pyrroloquinoline quinone has a regulatory role as a cofactor for dehydrogenases and an inducer of selected protein kinase activity in radiation resistance and DNA strand break repair in a radioresistant bacterium.

* Corresponding author. Mailing address: Molecular Biology Division, Bhabha Atomic Research Centre, Mumbai 400 085, India. Phone: 91-22-25595417. Fax: 91-22-25505151. E-mail: hsmisra{at}barc.gov.in

{triangledown} Published ahead of print on 28 March 2008.

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

Journal of Bacteriology, June 2008, p. 3948-3954, Vol. 190, No. 11
0021-9193/08/$08.00+0     doi:10.1128/JB.00026-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»