<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ramirez MV</submitter><funding>NIAID NIH HHS</funding><pagination>240</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3834876</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Molecular programs employed by Mycobacterium tuberculosis (Mtb) for the establishment of non-replicating persistence (NRP) are poorly understood. In order to investigate mechanisms regulating entry into NRP, we asked how cell cycle regulation is linked to downstream adaptations that ultimately result in NRP. Based on previous reports and our recent studies, we reason that, in order to establish NRP, cells are halted in the cell cycle at the point of septum formation by coupled regulatory mechanisms.&lt;h4>Results&lt;/h4>Using bioinformatic consensus modeling, we identified an alternative cell cycle regulatory element, Soj(Mtb) encoded by rv1708. Soj(Mtb) coordinates a regulatory mechanism involving cell cycle control at the point of septum formation and elicits the induction o</pubmed_abstract><journal>BMC microbiology</journal><pubmed_title>MazF6 toxin of Mycobacterium tuberculosis demonstrates antitoxin specificity and is coupled to regulation of cell growth by a Soj-like protein.</pubmed_title><pmcid>PMC3834876</pmcid><funding_grant_id>R01 AI055298</funding_grant_id><pubmed_authors>Dawson CC</pubmed_authors><pubmed_authors>Crew R</pubmed_authors><pubmed_authors>Slayden RA</pubmed_authors><pubmed_authors>England K</pubmed_authors><pubmed_authors>Ramirez MV</pubmed_authors></additional><is_claimable>false</is_claimable><name>MazF6 toxin of Mycobacterium tuberculosis demonstrates antitoxin specificity and is coupled to regulation of cell growth by a Soj-like protein.</name><description>&lt;h4>Background&lt;/h4>Molecular programs employed by Mycobacterium tuberculosis (Mtb) for the establishment of non-replicating persistence (NRP) are poorly understood. In order to investigate mechanisms regulating entry into NRP, we asked how cell cycle regulation is linked to downstream adaptations that ultimately result in NRP. Based on previous reports and our recent studies, we reason that, in order to establish NRP, cells are halted in the cell cycle at the point of septum formation by coupled regulatory mechanisms.&lt;h4>Results&lt;/h4>Using bioinformatic consensus modeling, we identified an alternative cell cycle regulatory element, Soj(Mtb) encoded by rv1708. Soj(Mtb) coordinates a regulatory mechanism involving cell cycle control at the point of septum formation and elicits the induction o</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Oct</publication><modification>2025-04-04T12:26:56.826Z</modification><creation>2019-03-27T03:08:58Z</creation></dates><accession>S-EPMC3834876</accession><cross_references><pubmed>24172039</pubmed><doi>10.1186/1471-2180-13-240</doi></cross_references></HashMap>