AI Article Synopsis

  • Cholera toxin (CT) causes cholera by binding to intestinal cells, and different types of fucosylated glycoconjugates are involved in this process.
  • Knocking out the B3GNT5 gene reduces CT binding in Colo205 cells but makes them more sensitive to CT intoxication, while increasing B3GNT5 levels can protect against CT.
  • Conversely, knocking out B3GALT5 increases production of certain glycoproteins that enhance CT binding and intoxication, highlighting the role of fucosylated glycoproteins as important receptors for CT.

Article Abstract

Cholera toxin (CT) is the etiological agent of cholera. Here we report that multiple classes of fucosylated glycoconjugates function in CT binding and intoxication of intestinal epithelial cells. In Colo205 cells, knockout (KO) of B3GNT5, which encodes an enzyme required for synthesis of lacto and neolacto series glycosphingolipids (GSLs), reduces CT binding but sensitizes cells to intoxication. Overexpressing B3GNT5 to generate more fucosylated GSLs confers protection against intoxication, indicating that fucosylated GSLs act as decoy receptors for CT. KO of B3GALT5 causes increased production of fucosylated O-linked and N-linked glycoproteins and leads to increased CT binding and intoxication. KO of B3GNT5 in B3GALT5-KO cells eliminates production of fucosylated GSLs but increases intoxication, identifying fucosylated glycoproteins as functional receptors for CT. These findings provide insight into the molecular determinants regulating CT sensitivity of host cells.

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Source
http://dx.doi.org/10.1038/s41589-024-01748-5DOI Listing

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