Reference - Detail
|Author||Koga M, Otsuka Y, Lemire S, Yonesaki T.|
|Title||Escherichia coli rnlA and rnlB compose a novel toxin-antitoxin system.|
RNase LS was originally identified as a potential antagonist of bacteriophage T4 infection. When T4 dmd is defective, RNase LS activity rapidly increases after T4 infection and cleaves T4 mRNAs to antagonize T4 reproduction. Here we show that rnlA, a structural gene of RNase LS, encodes a novel toxin, and that rnlB (formally yfjO), located immediately downstream of rnlA, encodes an antitoxin against RnlA. Ectopic expression of RnlA caused inhibition of cell growth and rapid degradation of mRNAs in ΔrnlAB cells. On the other hand, RnlB neutralized these RnlA effects. Furthermore, overexpression of RnlB in wild-type cells could completely suppress the growth defect of a T4 dmd mutant, that is, excess RnlB inhibited RNase LS activity. Pull-down analysis showed a specific interaction between RnlA and RnlB. Compared to RnlA, RnlB was extremely unstable, being degraded by ClpXP and Lon proteases, and this instability may increase RNase LS activity after T4 infection. All of these results suggested that rnlA-rnlB define a new toxin-antitoxin (TA) system.
|MeSH||Antitoxins / chemistry Antitoxins / genetics Antitoxins / immunology Antitoxins / metabolism* Bacterial Toxins / chemistry Bacterial Toxins / immunology Bacterial Toxins / metabolism* Escherichia coli K12 / cytology Escherichia coli K12 / genetics Escherichia coli K12 / metabolism* Escherichia coli Proteins / chemistry Escherichia coli Proteins / genetics Escherichia coli Proteins / immunology Escherichia coli Proteins / metabolism* Gene Expression Regulation, Bacterial Mutation Operon / genetics Protein Stability RNA Stability RNA, Messenger / chemistry RNA, Messenger / metabolism Ribonucleases / metabolism|
|WOS Category||GENETICS & HEREDITY|
|Prokaryotes E. coli||ME9062(BW25113)(Keio)|