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For an obligate pathogen such as\n            <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n            that has to complete successive cycles of transmission, infection, and disease in order to retain a foothold in the human population, this requires that genome replication and maintenance must be accomplished under the metabolic, immune, and antibiotic stresses encountered during passage through variable host environments. Comparative genomic analyses have established that chromosomal mutations enable\n            <jats:italic>M. tuberculosis<\/jats:italic>\n            to adapt to these stresses: the emergence of drug-resistant isolates provides direct evidence of this capacity, so too the well-documented genetic diversity among\n            <jats:italic>M. tuberculosis<\/jats:italic>\n            lineages across geographic loci, as well as the microvariation within individual patients that is increasingly observed as whole-genome sequencing methodologies are applied to clinical samples and tuberculosis (TB) disease models. However, the precise mutagenic mechanisms responsible for\n            <jats:italic>M. tuberculosis<\/jats:italic>\n            evolution and adaptation are poorly understood. Here, we summarize current knowledge of the machinery responsible for DNA replication in\n            <jats:italic>M. tuberculosis<\/jats:italic>\n            , and discuss the potential contribution of the expanded complement of mycobacterial DNA polymerases to mutagenesis. We also consider briefly the possible role of DNA replication\u2014in particular, its regulation and coordination with cell division\u2014in the ability of\n            <jats:italic>M. tuberculosis<\/jats:italic>\n            to withstand antibacterial stresses, including host immune effectors and antibiotics, through the generation at the population level of a tolerant state, or through the formation of a subpopulation of persister bacilli\u2014both of which might be relevant to the emergence and fixation of genetic drug resistance.\n          <\/jats:p>","DOI":"10.1128\/microbiolspec.tbtb2-0027-2016","type":"journal-article","created":{"date-parts":[[2017,3,31]],"date-time":"2017-03-31T12:58:05Z","timestamp":1490965085000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":49,"title":["DNA Replication in\n            <i>Mycobacterium tuberculosis<\/i>"],"prefix":"10.1128","volume":"5","author":[{"given":"Zanele","family":"Ditse","sequence":"first","affiliation":[{"name":"Centre for HIV and STIs, National Institute for Communicable Diseases of the National Health Laboratory Service, Johannesburg, 2131, South Africa"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meindert H.","family":"Lamers","sequence":"additional","affiliation":[{"name":"Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Digby F.","family":"Warner","sequence":"additional","affiliation":[{"name":"South African Medical Research Council (SAMRC)\/National Health Laboratory Services (NHLS)\/University of Cape Town (UCT) Molecular Mycobacteriology Research Unit, Department of Science and Technology (DST)\/National Research Foundation (NRF) Centre of Excellence for Biomedical TB Research, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Rondebosch 7700, South Africa"},{"name":"Institute of Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town; Rondebosch 7700 South Africa"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","unstructured":"Ambur OH Davidsen T Frye SA Balasingham SV Lagesen K Rognes T T\u00f8njum T. 2009. 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