#bacterial toxins

Glycolipid and Phospholipid

Which of the following glycolipids serves as a receptor for cholera toxin?

Specificity cholera toxin exemplifies glycan protein recognition medical consequence and cell biology tool. Vibrio cholerae AB5 holotoxin comprises catalytic A1 subunit ADP ribosyltransferase and homopentameric B subunits each containing binding pocket pentasaccharide GM1 Gal beta1-3 GalNAc beta1-4 Neu5Ac alpha2-3 Gal beta1-4 Glc ceramide. Key hydrogen bonds terminal galactose sialic acid provide nanomolar affinity positioning toxin on lipid rafts enterocytes small intestine. Raft mediated endocytosis delivers toxin retrograde trans Golgi ER where A1 ADP ribosylates Gs alpha arginine two hundred one locking GTP bound stimulating adenylate cyclase constitutively raising cAMP hundred fold opening CFTR chloride channels causing profuse watery diarrhea cholera gravis. Glucosylceramide lacks terminal sugars fails binding sulfatide distinct structure. GM1 knockout mice resist toxin GM1 supplemented liposomes detoxify pathogen. Interaction utilized neuronal tracing cholera toxin B HRP conjugates retrograde labeling dorsal root ganglia illustrating how glycolipid receptors dictate pathogenesis ABO blood group related susceptibility and toxin based tools for neuroscience and cell biology laboratory techniques widely taught in examinations.

Ref: Merritt et al., Protein Science 1994, Cholera toxin B subunit GM1 complex structure and pathogenesis.

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Cell Signaling GPCR Pathways - I

Pertussis toxin causes increased cAMP because it

Pertussis toxin ADP-ribosylates Gαi, preventing the inhibitory G protein from interacting with receptors and thereby blocking its ability to inhibit adenylyl cyclase. The resulting loss of tonic inhibition elevates cAMP levels and contributes to the pathogenesis of whooping cough. The toxin has also become a valuable experimental tool for identifying Gi-coupled pathways.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling GPCR Pathways - I

Pertussis toxin ADP-ribosylates

Pertussis toxin ADP-ribosylates Gαi, preventing the inhibitory G protein from interacting with receptors and thereby blocking its ability to inhibit adenylyl cyclase. The resulting loss of tonic inhibition elevates cAMP levels and contributes to the pathogenesis of whooping cough. The toxin has also become a valuable experimental tool for identifying Gi-coupled pathways.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling GPCR Pathways - I

Effect of cholera toxin on Gαs is

Cholera toxin catalyzes ADP-ribosylation of Gαs, locking the subunit in its GTP-bound active form by inhibiting GTPase activity. Persistent activation of adenylyl cyclase produces massive elevations of cAMP in intestinal epithelial cells, leading to continuous opening of chloride channels and the characteristic watery diarrhea of cholera. Careful

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling GPCR Pathways - I

Cholera toxin ADP-ribosylates which G-protein subunit?

Cholera toxin catalyzes ADP-ribosylation of Gαs, locking the subunit in its GTP-bound active form by inhibiting GTPase activity. Persistent activation of adenylyl cyclase produces massive elevations of cAMP in intestinal epithelial cells, leading to continuous opening of chloride channels and the characteristic watery diarrhea of cholera. Careful

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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