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However, the regulatory network associated with T6SS in\n              <jats:italic>A. baumannii<\/jats:italic>\n              remains poorly understood. Here, we identified an Mn\n              <jats:sup>2+<\/jats:sup>\n              -dependent post-transcriptional regulation of T6SS mediated by a bonafide small RNA, AbsR28.\n              <jats:italic>A. baumannii<\/jats:italic>\n              utilizes MumT, an Mn\n              <jats:sup>2+<\/jats:sup>\n              -uptake inner membrane transporter, for the uptake of extracellular Mn\n              <jats:sup>2+<\/jats:sup>\n              during oxidative stress. We demonstrate that the abundance of intracellular Mn\n              <jats:sup>2+<\/jats:sup>\n              enables complementary base pairing of AbsR28-\n              <jats:italic>tssM<\/jats:italic>\n              mRNA (that translates to TssM, one of the vital inner membrane components of T6SS), inducing RNase E-mediated degradation of\n              <jats:italic>tssM<\/jats:italic>\n              mRNA and resulting in T6SS repression. Thus, AbsR28 mediates a crosstalk between MumT and T6SS in\n              <jats:italic>A. baumannii<\/jats:italic>\n              .\n            <\/jats:p>\n            <jats:sec>\n              <jats:title>IMPORTANCE<\/jats:title>\n              <jats:p>\n                Small RNAs (sRNAs) are identified as critical components within the bacterial regulatory networks involved in fine regulation of virulence-associated factors. The sRNA-mediated regulation of type VI secretion system (T6SS) in\n                <jats:italic>Acinetobacter baumannii<\/jats:italic>\n                was unchartered. Previously, it was demonstrated that\n                <jats:italic>A. baumannii<\/jats:italic>\n                ATCC 17978 cells switch from T6\u2212 to T6+ phenotype, resulting in the loss of antibiotic resistance conferred by plasmid pAB3. Furthermore, the derivatives of pAB3 found in recent clinical isolates of\n                <jats:italic>A. baumannii<\/jats:italic>\n                harbor expanded antibiotic resistance genes and multiple determinants for virulence factors. Hence, the loss of this plasmid for T6SS activity renders\n                <jats:italic>A. baumannii<\/jats:italic>\n                T6+ cells susceptible to antibiotics and compromises their virulence. Our findings show how\n                <jats:italic>A. baumannii<\/jats:italic>\n                tends to inactivate T6SS through an sRNA-mediated regulation that relies on Mn\n                <jats:sup>2+<\/jats:sup>\n                and retains pAB3 during infection to retain antibiotic resistance genes carried on the plasmid.\n              <\/jats:p>\n            <\/jats:sec>\n          <\/jats:sec>","DOI":"10.1128\/mbio.03025-24","type":"journal-article","created":{"date-parts":[[2024,12,20]],"date-time":"2024-12-20T14:02:02Z","timestamp":1734703322000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":11,"title":["<i>Acinetobacter baumannii<\/i>\n            represses type VI secretion system through a manganese-dependent small RNA-mediated regulation"],"prefix":"10.1128","volume":"16","author":[{"given":"Somok","family":"Bhowmik","sequence":"first","affiliation":[{"name":"Department of Biosciences and 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