Bacillus licheniformis escapes from Myxococcus xanthus predation by deactivating myxovirescin A through enzymatic glucosylation.
Bacillus licheniformis escapes from Myxococcus xanthus predation by deactivating myxovirescin A through enzymatic glucosylation.
复制标题
DOI:
10.1111/1462-2920.14817
复制
发表时间:
2019-12
影响因子:
5.1
通讯作者:
Chuandong Wang;Xinli Liu;Peng Zhang;Yan Wang;Zhi-feng Li;Xun Li;Renqing Wang;Z. Shang;
中科院分区:
文献类型:
--
作者:
Chuandong Wang;Xinli Liu;Peng Zhang;Yan Wang;Zhi-feng Li;Xun Li;Renqing Wang;Z. Shang;
Myxococcus xanthus kills susceptible bacteria using myxovirescin A (TA) during predation. However, whether prey cells in nature can escape M. xanthus by developing resistance to TA is unknown. We observed that many field-isolated Bacillus licheniformis strains could survive encounters with M. xanthus, which was correlated to their TA resistance. A TA glycoside was identified in the broth of predation-resistant B. licheniformis J32 cocultured with M. xanthus, and a glycosyltransferase gene (yjiC) was up-regulated in J32 after the addition of TA. Hetero-expressed YjiC modified TA to a TA glucoside (TA-Gluc) by conjugating a glucose moiety to the C-21 hydroxyl group, and the resulting compound was identical to the TA glycoside present in the coculture broth. TA-Gluc exhibited diminished bactericidal activity due to its weaker binding with LspA, as suggested by in silico docking data. Heterologous expression of the yjiC gene conferred both TA and M. xanthus-predation resistance to the host E. coli cells. Furthermore, under predatory pressure, B. licheniformis Y071 rapidly developed predation-resistance by acquiring TA-resistance through the overexpression of yjiC and lspA genes. These results suggest that M. xanthus predation resistance in B. licheniformis is due to the TA deactivation by glucosylation, which is induced in a predator-mediated manner. This article is protected by copyright. All rights reserved.