<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang Y</submitter><funding>American Heart Association</funding><pagination>e00743-17</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5869477</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>200(8)</volume><pubmed_abstract>Clustered regularly interspaced short palindromic repeats (CRISPR) and the CRISPR-associated proteins (Cas) provide bacteria and archaea with adaptive immunity to specific DNA invaders. &lt;i>Mycobacterium tuberculosis&lt;/i> encodes a type III CRISPR-Cas system that has not been experimentally explored. In this study, we found that the CRISPR-Cas systems of both &lt;i>M. tuberculosis&lt;/i> and &lt;i>Mycobacterium bovis&lt;/i> BCG were highly upregulated by deletion of Rv2837c (&lt;i>cnpB&lt;/i>), which encodes a multifunctional protein that hydrolyzes cyclic di-AMP (c-di-AMP), cyclic di-GMP (c-di-GMP), and nanoRNAs (short oligonucleotides of 5 or fewer residues). By using genetic and biochemical approaches, we demonstrated that the CnpB-controlled transcriptional regulation of the CRISPR-Cas system is mediated </pubmed_abstract><journal>Journal of bacteriology</journal><pubmed_title>Regulation of the CRISPR-Associated Genes by Rv2837c (CnpB) via an Orn-Like Activity in Tuberculosis Complex Mycobacteria.</pubmed_title><pmcid>PMC5869477</pmcid><funding_grant_id>12SDG12080067</funding_grant_id><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Bai G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulation of the CRISPR-Associated Genes by Rv2837c (CnpB) via an Orn-Like Activity in Tuberculosis Complex Mycobacteria.</name><description>Clustered regularly interspaced short palindromic repeats (CRISPR) and the CRISPR-associated proteins (Cas) provide bacteria and archaea with adaptive immunity to specific DNA invaders. &lt;i>Mycobacterium tuberculosis&lt;/i> encodes a type III CRISPR-Cas system that has not been experimentally explored. In this study, we found that the CRISPR-Cas systems of both &lt;i>M. tuberculosis&lt;/i> and &lt;i>Mycobacterium bovis&lt;/i> BCG were highly upregulated by deletion of Rv2837c (&lt;i>cnpB&lt;/i>), which encodes a multifunctional protein that hydrolyzes cyclic di-AMP (c-di-AMP), cyclic di-GMP (c-di-GMP), and nanoRNAs (short oligonucleotides of 5 or fewer residues). By using genetic and biochemical approaches, we demonstrated that the CnpB-controlled transcriptional regulation of the CRISPR-Cas system is mediated </description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Apr</publication><modification>2026-04-29T16:59:13.975Z</modification><creation>2019-03-26T23:57:04Z</creation></dates><accession>S-EPMC5869477</accession><cross_references><pubmed>29378893</pubmed><doi>10.1128/JB.00743-17</doi><doi>10.1128/jb.00743-17</doi></cross_references></HashMap>