ArticlePloS one2014
Either non-homologous ends joining or homologous recombination is required to repair double-strand breaks in the genome of macrophage-internalized Mycobacterium tuberculosis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Dual transcriptomic analysis unraveling the immune landscape and host-pathogen interactions duringiScience · 2025Article
- Oligomerisation of Ku from Mycobacterium tuberculosis promotes DNA synapsis.Nature communications · 2025Article
- Prokaryotic homeostasis - a solution to thrive and survive.Frontiers in molecular biosciences · 2025Review
- Mycobacterium tuberculosis Ku Stimulates Multi-round DNA Unwinding by UvrD1 Monomers.Journal of molecular biology · 2024Article
- Defects in DNA double-strand break repair resensitize antibiotic-resistant Escherichia coli to multiple bactericidal antibiotics.MicrobiologyOpen · 2022Article
- The Orphan Response Regulator Rv3143 Modulates the Activity of the NADH Dehydrogenase Complex (Nuo) inFrontiers in cellular and infection microbiology · 2022Article
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- LigD: A Structural Guide to the Multi-Tool of Bacterial Non-Homologous End Joining.Frontiers in molecular biosciences · 2021Review
- Mycobacterium tuberculosis and Mycobacterium marinum non-homologous end-joining proteins can function together to join DNA ends in Escherichia coli.Mutagenesis · 2017Article
- Deletion of a dehydratase important for intracellular growth and cording renders rough Mycobacterium abscessus avirulent.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Methodological and Clinical Aspects of the Molecular Epidemiology of Mycobacterium tuberculosis and Other Mycobacteria.Clinical microbiology reviews · 2016Review
- Caveolin-1 is Associated with Tumor Progression and Confers a Multi-Modality Resistance Phenotype in Pancreatic Cancer.Scientific reports · 2015Article
- Bacterial nonhomologous end joining requires teamwork.Journal of bacteriology · 2014Article
- Deficiency of double-strand DNA break repair does not impair Mycobacterium tuberculosis virulence in multiple animal models of infection.Infection and immunity · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intracellular pathogen Mycobacterium tuberculosis (Mtb) is constantly exposed to a multitude of hostile conditions and is confronted by a variety of potentially DNA-damaging assaults in vivo, primarily from host-generated antimicrobial toxic radicals. Exposure to reactive nitrogen species and/or reactive oxygen species causes different types of DNA damage, including oxidation, depurination, methylation and deamination, that can result in single- or double-strand breaks (DSBs). These breaks affect the integrity of the whole genome and, when left unrepaired, can lead to cell death. Here, we investigated the role of the DSB repair pathways, homologous recombination (HR) and non-homologous ends joining (NHEJ), in the survival of Mtb inside macrophages. To this end, we constructed Mtb strains defective for HR (ΔrecA), NHEJ [Δ(ku,ligD)], or both DSB repair systems [Δ(ku,ligD,recA)]. Experiments using these strains revealed that either HR or NHEJ is sufficient for the survival and propagation of tubercle bacilli inside macrophages. Inhibition of nitric oxide or superoxide anion production with L-NIL or apocynin, respectively, enabled the Δ(ku,ligD,recA) mutant strain lacking both systems to survive intracellularly. Complementation of the Δ(ku,ligD,recA) mutant with an intact recA or ku-ligD rescued the ability of Mtb to propagate inside macrophages.
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