Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.

Tuberculosis caused by Mycobacterium tuberculosis (Mtb) is a significant public health concern, exacerbated by the emergence of drug-resistant TB. To combat the host's dynamic environment, Mtb encodes multiple DNA repair enzymes that play a critical role in maintaining genomic integrity. Mtb po...

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Main Authors: Saba Naz, Shruti Dabral, Sathya Narayanan Nagarajan, Divya Arora, Lakshya Veer Singh, Pradeep Kumar, Yogendra Singh, Dhiraj Kumar, Umesh Varshney, Vinay Kumar Nandicoori
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2021-03-01
Series:PLoS Pathogens
Online Access:https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1009452&type=printable
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author Saba Naz
Shruti Dabral
Sathya Narayanan Nagarajan
Divya Arora
Lakshya Veer Singh
Pradeep Kumar
Yogendra Singh
Dhiraj Kumar
Umesh Varshney
Vinay Kumar Nandicoori
author_facet Saba Naz
Shruti Dabral
Sathya Narayanan Nagarajan
Divya Arora
Lakshya Veer Singh
Pradeep Kumar
Yogendra Singh
Dhiraj Kumar
Umesh Varshney
Vinay Kumar Nandicoori
author_sort Saba Naz
collection DOAJ
description Tuberculosis caused by Mycobacterium tuberculosis (Mtb) is a significant public health concern, exacerbated by the emergence of drug-resistant TB. To combat the host's dynamic environment, Mtb encodes multiple DNA repair enzymes that play a critical role in maintaining genomic integrity. Mtb possesses a GC-rich genome, rendering it highly susceptible to cytosine deaminations, resulting in the occurrence of uracils in the DNA. UDGs encoded by ung and udgB initiate the repair; hence we investigated the biological impact of deleting UDGs in the adaptation of pathogen. We generated gene replacement mutants of uracil DNA glycosylases, individually (RvΔung, RvΔudgB) or together (RvΔdKO). The double KO mutant, RvΔdKO exhibited remarkably higher spontaneous mutation rate, in the presence of antibiotics. Interestingly, RvΔdKO showed higher survival rates in guinea pigs and accumulated large number of SNPs as revealed by whole-genome sequence analysis. Competition assays revealed the superior fitness of RvΔdKO over Rv, both in ex vivo and in vivo conditions. We propose that compromised DNA repair results in the accumulation of mutations, and a subset of these drives adaptation in the host. Importantly, this property allowed us to utilize RvΔdKO for the facile identification of drug targets.
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institution OA Journals
issn 1553-7366
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language English
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record_format Article
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spelling doaj-art-ae7f2b4093a74f83a8f22169e5497d402025-08-20T02:01:05ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742021-03-01173e100945210.1371/journal.ppat.1009452Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.Saba NazShruti DabralSathya Narayanan NagarajanDivya AroraLakshya Veer SinghPradeep KumarYogendra SinghDhiraj KumarUmesh VarshneyVinay Kumar NandicooriTuberculosis caused by Mycobacterium tuberculosis (Mtb) is a significant public health concern, exacerbated by the emergence of drug-resistant TB. To combat the host's dynamic environment, Mtb encodes multiple DNA repair enzymes that play a critical role in maintaining genomic integrity. Mtb possesses a GC-rich genome, rendering it highly susceptible to cytosine deaminations, resulting in the occurrence of uracils in the DNA. UDGs encoded by ung and udgB initiate the repair; hence we investigated the biological impact of deleting UDGs in the adaptation of pathogen. We generated gene replacement mutants of uracil DNA glycosylases, individually (RvΔung, RvΔudgB) or together (RvΔdKO). The double KO mutant, RvΔdKO exhibited remarkably higher spontaneous mutation rate, in the presence of antibiotics. Interestingly, RvΔdKO showed higher survival rates in guinea pigs and accumulated large number of SNPs as revealed by whole-genome sequence analysis. Competition assays revealed the superior fitness of RvΔdKO over Rv, both in ex vivo and in vivo conditions. We propose that compromised DNA repair results in the accumulation of mutations, and a subset of these drives adaptation in the host. Importantly, this property allowed us to utilize RvΔdKO for the facile identification of drug targets.https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1009452&type=printable
spellingShingle Saba Naz
Shruti Dabral
Sathya Narayanan Nagarajan
Divya Arora
Lakshya Veer Singh
Pradeep Kumar
Yogendra Singh
Dhiraj Kumar
Umesh Varshney
Vinay Kumar Nandicoori
Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.
PLoS Pathogens
title Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.
title_full Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.
title_fullStr Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.
title_full_unstemmed Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.
title_short Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.
title_sort compromised base excision repair pathway in mycobacterium tuberculosis imparts superior adaptability in the host
url https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1009452&type=printable
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