<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>5(6)</volume><submitter>Jakkala K</submitter><funding>DBT-IISc Partnership Programme</funding><pubmed_abstract>The emergence of antibiotic genetic resisters of pathogenic bacteria poses a major public health challenge. The mechanism by which bacterial antibiotic genetic resister clones formed &lt;i>de novo&lt;/i> multiply and establish a resister population remained unknown. Here, we delineated the unique mode of cell division of the antibiotic genetic resisters of &lt;i>Mycobacterium smegmatis&lt;/i> and &lt;i>Mycobacterium tuberculosis&lt;/i> formed &lt;i>de novo&lt;/i> from the population surviving in the presence of bactericidal concentrations of rifampicin or moxifloxacin. The cells in the rifampicin/moxifloxacin-surviving population generated elevated levels of hydroxyl radical-inflicting mutations. The genetic mutants selected against rifampicin/moxifloxacin became multinucleated and multiseptated and developed mul</pubmed_abstract><journal>mSphere</journal><pagination>e00994-20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7677009</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Unique Mode of Cell Division by the Mycobacterial Genetic Resister Clones Emerging &lt;i>De Novo&lt;/i> from the Antibiotic-Surviving Population.</pubmed_title><pmcid>PMC7677009</pmcid><pubmed_authors>Pradhan A</pubmed_authors><pubmed_authors>Ajitkumar P</pubmed_authors><pubmed_authors>Sharan D</pubmed_authors><pubmed_authors>Paul A</pubmed_authors><pubmed_authors>Swaminath S</pubmed_authors><pubmed_authors>Nair RR</pubmed_authors><pubmed_authors>Jakkala K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Unique Mode of Cell Division by the Mycobacterial Genetic Resister Clones Emerging &lt;i>De Novo&lt;/i> from the Antibiotic-Surviving Population.</name><description>The emergence of antibiotic genetic resisters of pathogenic bacteria poses a major public health challenge. The mechanism by which bacterial antibiotic genetic resister clones formed &lt;i>de novo&lt;/i> multiply and establish a resister population remained unknown. Here, we delineated the unique mode of cell division of the antibiotic genetic resisters of &lt;i>Mycobacterium smegmatis&lt;/i> and &lt;i>Mycobacterium tuberculosis&lt;/i> formed &lt;i>de novo&lt;/i> from the population surviving in the presence of bactericidal concentrations of rifampicin or moxifloxacin. The cells in the rifampicin/moxifloxacin-surviving population generated elevated levels of hydroxyl radical-inflicting mutations. The genetic mutants selected against rifampicin/moxifloxacin became multinucleated and multiseptated and developed mul</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Nov</publication><modification>2026-06-06T03:30:45.92Z</modification><creation>2021-02-20T02:47:44Z</creation></dates><accession>S-EPMC7677009</accession><cross_references><pubmed>33208519</pubmed><doi>10.1128/mSphere.00994-20</doi></cross_references></HashMap>