YoeB toxin is activated during thermal stress

摘要: Type II toxin-antitoxin (TA) modules are thought to mediate stress-responses by temporarily suppressing protein synthesis while cells redirect transcription adapt environmental change. Here, we show that YoeB, a ribosome-dependent mRNase toxin, is activated in Escherichia coli grown at elevated temperatures. YoeB activation dependent on Lon protease, suggesting thermal stress promotes increased degradation of the YefM antitoxin. Though efficiently degraded response overproduction, find antigen levels do not increase during heat shock, indicating another mechanism accounts for temperature-induced proteolysis. These observations suggest YefM/YoeB functions adaptation temperature stress. However, this distinct from previously described models TA function. First, activity maintained over several hours culture 42°C, transient. Moreover, heat-activated does induce growth arrest nor it suppress global synthesis. In fact, E. coli proliferate more rapidly temperatures and instantaneously accelerate their rate acute shock. We propose may serve quality control function, facilitating recycling stalled translation complexes through ribosome rescue pathways.