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

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.