active transport and cholera

Grade 12, eh? Best I can do is forward a friend's website that might help with answering this question.

Here's the exert that will help with the understanding of cholera toxin:

The enterotoxin works by activating adenylate cyclase in the epithelial cells. More specifically, it inhibits GTPase enzyme activity so that GDP (an inhibitory molecule) cannot replace the activated G protein which has GTP bound to it in its active state during signal transduction. The activated G protein goes on to activate adenylyl cyclase, producing large amounts of another chemical compound called cAMP. cAMP then activates protein kinase A, an enzyme that induces several different cellular responses, including the release of ions. cAMP also opens plasma membrane calcium channels, so that large amounts of calcium are released into the intestines, leading to an increase in water loss. Cholera toxin modifies the G protein by adding an ADP-ribosyl group to it. This prevents the enzyme GTPase, as mentioned earlier, from hydrolyzing the activated the G protein to a deactivated state which has GDP bound to it, as opposed to GTP. As a result, if the G protein is constantly active, there is persistent activation of adenylyl cyclase and, in turn, a nonregulated rise of intracellular cAMP.

The link: http://www.ppdictionary.com/bacteria/gnbac/cholerae.htm

Good luck, bio_lover