Cell death signaling in Anopheles gambiae initiated by Bacillus thuringiensis Cry4B toxin involves Na⁺/K⁺ ATPase.

ABSTRACT: Identifying the mechanisms by which bacterial pathogens kill host cells is fundamental to understanding how to control and prevent human and animal disease. In the case of Bacillus thuringiensis (Bt), such knowledge is critical to using the bacterium to kill insect vectors that transmit human and animal disease. For the Cry4B toxin produced by Bt, its capacity to kill Anopheles gambiae, the primary mosquito vector of malaria, is the consequence of a variety of signaling activities. We show here that Cry4B, acting as first messenger, binds specifically to the bitopic cadherin BT-R₃ G-protein-coupled receptor (GPCR) localized in the midgut of A. gambiae, activating the downstream second messenger cyclic adenosine monophosphate (cAMP). The direct result of the

SUBMITTER: Liu L 

PROVIDER: S-EPMC10621475 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature