Glutamine‐rich toxic proteins GrtA, GrtB and GrtC together with the antisense RNA AsgR constitute a toxin–antitoxin‐like system in Corynebacterium glutamicum. Issue 5 (19th April 2018)

• Record Type: Journal Article
• Authors: Maeda, Tomoya; Tanaka, Yuya; Inui, Masayuki
• Is Part Of: Molecular microbiology. Volume 108:Issue 5(2018)
• Page Start: 578
• Page End: 594
• Publication Date: 2018-04-19
• Subjects: Molecular microbiology -- Periodicals; 572.829
• DOI: 10.1111/mmi.13951
• Languages: English
• ISSNs: 0950-382X

Abstract

Summary: The Corynebacterium glutamicum R grtA (cgR_2936), grtB (cgR_2934) and grtC (cgR_2933) genes were identified as paralogs encoding glutamine‐rich toxic proteins. We also identified a new antisense small RNA AsgR (antisense sRNA for grtA ) that overlaps the 3′ end of the grtA gene. Single over‐expressions of grtA, grtB and grtC resulted in complete inhibition of Escherichia coli cell growth. This growth was rescued by co‐expression of AsgR. Similar effects were observed in C. glutamicum, although the toxicities of these proteins were moderate. Inhibition of AsgR transcription resulted in increased levels and prolonged half‐lives of grtA, grtB and grtC mRNAs. We also found that the expression levels of grtA, grtB and grtC were increased in an RNase III deletion mutant. Primer extension analysis revealed the RNase III cleavage site to be in the 3′ untranslated region (3′‐UTR) of the grtA mRNA. The expression levels of grtA, grtB and grtC were increased after exposure to several stresses, including heat shock, treatment with penicillin G, lysozyme or H2 O2 . The deletions of grtABC and asgR genes resulted in decreased survival rate under several stresses. These results indicate that GrtABC and AsgR constitute a type I toxin–antitoxin‐like system in C. glutamicum . Abstract : We report a new type I toxin‐antitoxin system in Corynebacterium glutamicum which is a workhorse of amino acid production. The TA system is composed of three repeated glutamine‐rich proteins encoded by grtABC genes and an antisense small RNA AsgR. The expression of grtABC is induced by several stressors while the repression of grtABC is achieved by the grtA ‐AsgR duplex formation at the 3′ untranslated region (3′‐UTR) and subsequent degradation by RNase III.