Department of Molecular Bacteriology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan.
Center for Infectious Disease Education and Research, Osaka University, Suita, Osaka 565-0871, Japan.
Proc Natl Acad Sci U S A. 2023 Oct 3;120(40):e2308260120. doi: 10.1073/pnas.2308260120. Epub 2023 Sep 25.
The pathogenic bacteria and cause pertussis (whooping cough) and pertussis-like disease, respectively, both of which are characterized by paroxysmal coughing. We previously reported that pertussis toxin (PTx), which inactivates heterotrimeric GTPases of the G family through ADP-ribosylation of their α subunits, causes coughing in combination with Vag8 and lipid A in infection. In contrast, the mechanism of cough induced by , which produces Vag8 and lipopolysaccharide (LPS) containing lipid A, but not PTx, remained to be elucidated. Here, we show that a toxin we named deacylating autotransporter toxin (DAT) of inactivates heterotrimeric G GTPases through demyristoylation of their α subunits and contributes to cough production along with Vag8 and LPS. These results indicate that DAT plays a role in infection in place of PTx.
该致病菌分别引起百日咳（百日咳）和类似百日咳的疾病，这两种疾病均以阵发性咳嗽为特征。我们之前报道过，百日咳毒素（PTx）通过其α亚基的 ADP-核糖基化使 G 家族的异三聚体 GTP 酶失活，与 Vag8 和脂质 A 一起在感染中引起咳嗽。相比之下，产生 Vag8 和脂多糖（LPS）但不产生 PTx 的 引起咳嗽的机制仍有待阐明。在这里，我们表明，我们命名为 的去酰化自转运毒素（DAT）通过其α亚基的脱酰基化使异三聚体 G GTP 酶失活，并与 Vag8 和 LPS 一起促进咳嗽的产生。这些结果表明 DAT 在代替 PTx 参与 感染。
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