<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hsueh BY</submitter><funding>NIAID NIH HHS</funding><funding>Michigan State University</funding><funding>U.S. Department of Health &amp;amp; Human Services | National Institutes of Health</funding><funding>NIGMS NIH HHS</funding><funding>National Science Foundation</funding><pagination>1210-1220</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9830645</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7(8)</volume><pubmed_abstract>Vibrio cholerae biotype El Tor is perpetuating the longest cholera pandemic in recorded history. The genomic islands VSP-1 and VSP-2 distinguish El Tor from previous pandemic V. cholerae strains. Using a co-occurrence analysis of VSP genes in >200,000 bacterial genomes we built gene networks to infer biological functions encoded in these islands. This revealed that dncV, a component of the cyclic-oligonucleotide-based anti-phage signalling system (CBASS) anti-phage defence system, co-occurs with an uncharacterized gene vc0175 that we rename avcD for anti-viral cytodine deaminase. We show that AvcD is a deoxycytidylate deaminase and that its activity is post-translationally inhibited by a non-coding RNA named AvcI. AvcID and bacterial homologues protect bacterial populations against phage i</pubmed_abstract><journal>Nature microbiology</journal><pubmed_title>Phage defence by deaminase-mediated depletion of deoxynucleotides in bacteria.</pubmed_title><pmcid>PMC9830645</pmcid><funding_grant_id>AI143098</funding_grant_id><funding_grant_id>R41 AI143098</funding_grant_id><funding_grant_id>R35 GM139537</funding_grant_id><funding_grant_id>R01 GM110444</funding_grant_id><funding_grant_id>GM109259</funding_grant_id><funding_grant_id>R01 GM110185</funding_grant_id><funding_grant_id>R01 AI158433</funding_grant_id><funding_grant_id>GM139537</funding_grant_id><funding_grant_id>GM110444</funding_grant_id><funding_grant_id>1842399</funding_grant_id><funding_grant_id>R01 GM109259</funding_grant_id><funding_grant_id>AI158433</funding_grant_id><funding_grant_id>DBI-0939454</funding_grant_id><funding_grant_id>GM110185</funding_grant_id><funding_grant_id>1750125</funding_grant_id><pubmed_authors>Elg CA</pubmed_authors><pubmed_authors>Neiditch MB</pubmed_authors><pubmed_authors>Hsueh BY</pubmed_authors><pubmed_authors>Parent KN</pubmed_authors><pubmed_authors>Ridenhour BJ</pubmed_authors><pubmed_authors>Top EM</pubmed_authors><pubmed_authors>Waters CM</pubmed_authors><pubmed_authors>Severin GB</pubmed_authors><pubmed_authors>Wessel AJ</pubmed_authors><pubmed_authors>Ravi J</pubmed_authors><pubmed_authors>Kant A</pubmed_authors><pubmed_authors>Dover JA</pubmed_authors><pubmed_authors>Waldron EJ</pubmed_authors><pubmed_authors>Rhoades CR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Phage defence by deaminase-mediated depletion of deoxynucleotides in bacteria.</name><description>Vibrio cholerae biotype El Tor is perpetuating the longest cholera pandemic in recorded history. The genomic islands VSP-1 and VSP-2 distinguish El Tor from previous pandemic V. cholerae strains. Using a co-occurrence analysis of VSP genes in >200,000 bacterial genomes we built gene networks to infer biological functions encoded in these islands. This revealed that dncV, a component of the cyclic-oligonucleotide-based anti-phage signalling system (CBASS) anti-phage defence system, co-occurs with an uncharacterized gene vc0175 that we rename avcD for anti-viral cytodine deaminase. We show that AvcD is a deoxycytidylate deaminase and that its activity is post-translationally inhibited by a non-coding RNA named AvcI. AvcID and bacterial homologues protect bacterial populations against phage i</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Aug</publication><modification>2026-06-04T05:49:38.779Z</modification><creation>2025-04-19T13:31:48.829Z</creation></dates><accession>S-EPMC9830645</accession><cross_references><pubmed>35817890</pubmed><doi>10.1038/s41564-022-01162-4</doi></cross_references></HashMap>