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

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 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.

Keywords: Bordetella parapertussis; DAT; Gi GTPases; cough; demyristoylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bordetella parapertussis*
  • Bordetella pertussis
  • Cough
  • Humans
  • Lipid A
  • Lipopolysaccharides / toxicity
  • Pertussis Toxin
  • Toxins, Biological*
  • Type V Secretion Systems
  • Whooping Cough*


  • Type V Secretion Systems
  • Lipid A
  • Lipopolysaccharides
  • Pertussis Toxin
  • Toxins, Biological