ArticlePLoS pathogens2021
Compromised base excision repair pathway in Mycobacterium tuberculosis imparts superior adaptability in the host.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Usnic Acid Derivatives as Inhibitors ofInternational journal of molecular sciences · 2026Article
- Recent Characterization of Key Proteins to Combat Tuberculosis.Advances in experimental medicine and biology · 2026Review
- Genome wide analyses reveal the role of mutator phenotypes in Mycobacterium tuberculosis drug resistance emergence.npj antimicrobials and resistance · 2025Article
- GWAS and functional studies suggest a role for altered DNA repair in the evolution of drug resistance ineLife · 2023Article
- Protocol forSTAR protocols · 2022Article
- Distinctive roles of translesion polymerases DinB1 and DnaE2 in diversification of the mycobacterial genome through substitution and frameshift mutagenesis.Nature communications · 2022Article
- Root-knot nematodes (Meloidogyne spp.) a threat to agriculture in Mexico: biology, current control strategies, and perspectives.World journal of microbiology & biotechnology · 2022Review
- Division of labor between SOS and PafBC in mycobacterial DNA repair and mutagenesis.Nucleic acids research · 2021Article
- Screening of Compounds for Anti-tuberculosis Activity, andFrontiers in microbiology · 2021Article
- Transcriptional Response ofFrontiers in microbiology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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