Vibrio cholerae ensures function of host proteins required for virulence through consumption of luminal methionine sulfoxide
Fig 3
Decreased consumption of methionine sulfoxide (MetO) by the V. cholerae ΔgcvT mutant attenuates virulence by promoting intestinal lipid mobilization and insulin signaling.
(A) Survival curves of flies fed LB broth inoculated with wild-type V. cholerae (WT) supplemented with 50 mM methionine (Met) or 25 mM and 50 mM methionine sulfoxide (MetO). (B) Bacterial burden of flies measured in colony forming units (cfu) after ingestion of LB broth supplemented with 25mM and 50mM methionine sulfoxide (MetO) and inoculated with wild-type V. cholerae (WT). (C) Enumeration of PH3+ cells in the intestines of flies fed PBS or PBS supplemented with 50 mM methionine (Met) and 50 mM methionine sulfoxide (MetO) for 72h. (D) Nile red staining of neutral lipids in the fat body and intestine of flies fed LB broth or LB broth inoculated with wild-type V. cholerae (WT) supplemented with methionine (Met) or methionine sulfoxide (MetO). (E) Quantification of midgut cells containing lipid droplets. (F) Western blot analysis of phosphorylated AKT (pAKT) or total AKT levels in whole flies fed LB broth alone or inoculated with wild-type V. cholerae (WT) supplemented with methionine (Met) or methionine sulfoxide (MetO). For pooled data, the mean and SD are shown. Pairwise statistical significance was calculated using a student’s t-test (*p<0.05, **p<0.01, ***p<0.001).
