Distinct mechanisms of DNA repair in mycobacteria and their implications in attenuation of the pathogen growth

Kurthkoti, Krishna and Varshney, Umesh (2012) Distinct mechanisms of DNA repair in mycobacteria and their implications in attenuation of the pathogen growth. In: MECHANISMS OF AGEING AND DEVELOPMENT, 133 (4, SI). pp. 138-146.

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Abstract

About a third of the human population is estimated to be infected with Mycobacterium tuberculosis. Emergence of drug resistant strains and the protracted treatment strategies have compelled the scientific community to identify newer drug targets, and to develop newer vaccines. In the host macrophages, the bacterium survives within an environment rich in reactive nitrogen and oxygen species capable of damaging its genome. Therefore, for its successful persistence in the host, the pathogen must need robust DNA repair mechanisms. Analysis of M. tuberculosis genome sequence revealed that it lacks mismatch repair pathway suggesting a greater role for other DNA repair pathways such as the nucleotide excision repair, and base excision repair pathways. In this article, we summarize the outcome of research involving these two repair pathways in mycobacteria focusing primarily on our own efforts. Our findings, using Mycobacterium smegmatis model, suggest that deficiency of various DNA repair functions in single or in combinations severely compromises their DNA repair capacity and attenuates their growth under conditions typically encountered in macrophages. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

Item Type:	Journal Article
Publication:	MECHANISMS OF AGEING AND DEVELOPMENT
Publisher:	ELSEVIER IRELAND LTD
Additional Information:	Indo-US Workshop on Base Excision DNA Repair, Brain Function and Aging, Hyderabad, INDIA, JAN, 2011
Keywords:	Copyright for this article belongs to Elsevier
Department/Centre:	Division of Biological Sciences > Microbiology & Cell Biology
Date Deposited:	04 Jul 2012 12:52
Last Modified:	04 Jul 2012 12:52
URI:	http://eprints.iisc.ac.in/id/eprint/44774

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