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DAT, deacylating autotransporter toxin, from Bordetella parapertussis demyristoylates Gαi GTPases and contributes to cough.


ABSTRACT: The pathogenic bacteria Bordetella pertussis and Bordetella parapertussis 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 Gi family through ADP-ribosylation of their α subunits, causes coughing in combination with Vag8 and lipid A in B. pertussis infection. In contrast, the mechanism of cough induced by B. parapertussis, 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 B. parapertussis inactivates heterotrimeric Gi 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 B. parapertussis infection in place of PTx.

SUBMITTER: Hiramatsu Y 

PROVIDER: S-EPMC10556565 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature

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DAT, deacylating autotransporter toxin, from <i>Bordetella parapertussis</i> demyristoylates Gα<sub>i</sub> GTPases and contributes to cough.

Hiramatsu Yukihiro Y   Nishida Takashi T   Ota Natsuko N   Tamaki Yuki Y   Nugraha Dendi K DK   Horiguchi Yasuhiko Y  

Proceedings of the National Academy of Sciences of the United States of America 20230925 40


The pathogenic bacteria <i>Bordetella pertussis</i> and <i>Bordetella parapertussis</i> 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<sub>i</sub> family through ADP-ribosylation of their α subunits, causes coughing in combination with Vag8 and lipid A in <i>B. pertussis</i> infection. In contrast, the mechanism o  ...[more]

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