Abstract
Pore-forming toxins (PFTs) are abundant bacterial virulence factors that attack host cell plasma membranes. Host defense mechanisms against PFTs described to date all function in the host tissue that is directly attacked by the PFT. Here we characterize a rapid and fully penetrant cessation of feeding of Caenorhabditis elegans in response to PFT attack. We demonstrate via analyses of C. elegans mutants that inhibition of feeding by PFT requires the neuronal G protein Goα subunit goa-1, and that maintenance of this response requires neuronally expressed calcium activator for protein secretion (CAPS) homolog unc-31. Independently from their role in feeding cessation, we find that goa-1 and unc-31 are additionally required for immune protection against PFTs. We thus demonstrate that the behavioral and immune responses to bacterial PFT attack involve the cross-talk between the nervous system and the cells directly under attack.
Highlights
Bacterial infectious diseases rank among the top leading causes of death worldwide
pore-forming toxins (PFTs) rapidly and reversibly induce feeding cessation To measure the kinetics of feeding inhibition by PFT, we determined fractions of animals feeding after various exposure times to Cry5B expressed from Escherichia coli, C. elegans’ normal lab food source
Inhibition of feeding induced by Cry5B, V. cholerae cytolysin (VCC) and Cry21A follow very similar kinetics (Fig. 1A, C, S1A), and it appears that rapid inhibition of feeding is part of a generalized response of C. elegans to smallpore bacterial PFTs
Summary
Bacterial infectious diseases rank among the top leading causes of death worldwide. Cells possess PFT-defense mechanisms involved in membrane resealing, as well as various molecular defenses [6,7,8,9,10,11,12,13,14]. Many genes involved in protection against PFTs were discovered in C. elegans using the PFT Cry5B and, where tested, were found to have conserved roles in mammalian cells [7,11,14]. As we have previously noted [13,15], the PFT Cry5B causes an inhibition of feeding behavior in C. elegans, suggestive of a neuronal component to PFT responses
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