Question

€ → C .ap2020.collegeboard.org/Praott-aa857320- glucagon (a) A cell where PKB is always active has a mutation that results in the permanent activation of GSK3. Based on the information in Figure 2, predict the effect of this mutation on the activity of glycogen synthase. (b) Justify your prediction in part (a). Describe the process that results in the activation of multiple copies of PKB in response to the binding of a single molecule of insulin to its receptor. (d) Explain why insulin can stimulate the activation of PKB but not the activation of PK. () Explain why an increase in glycogen phosphorylase activity might result in an increase in O2 consumption in the cell. (1) A certain type of tumor results in the overproduction of glucagon. Researchers claim that treatment with insulin can counteract the effects of the excess glucagon on the pathway shown in Figure 2. Provide reasoning to justify the researchers' claim. Time Left to Submit Work 0:17:34

Answer 1

a) Glycogen synthase will remain inactivated as it is constitutively inhibited by GSK3.

b) Insulin signaling leads to activation of PKB. PKB inhibits GSK3. Here the mutation causes PKB not to inactivate GSK3. Thus GSK3 remains active always. GSK3 inturn inactive glycogen synthase. Thus constitutive activation of GSK3 doesn't allow glycogen synthase to become activated.

c) Insulin binding to its receptor causes autophosphorylation of the insulin receptor. This leads to docking of IRS-1 to the phosphorylated c terminal region of the receptor. IRS-1 is also phosphorylated. Activated IRS-1 activate Pi3K, which in turn converts PIP2 into PIP3. PKB bound to PIP3 is then phosphorylated and activated by PDK1.

The activation multiple molecules of IRS-1 occur in this signalling pathway. Multiple IRS-1 activates multiple PIP3 and ultimately multiple numbers of PKB are activated.

d) Insulin signalling pathway activates PI3K bound PKB. Other PKs are not bounded to the Pi3K. Thus insulin signalling doesn't activate other PKs.

e) Overactivation of glycogen phosphorylase leads to convertion of more glycogen molecules into glucose-1-phosphate. G-1-P is converted into G-6-P which enters glycolysis. Ultimately this pathway ends up with completion of cellular respiration, synthesis of ATPs and consumption of O2.

f) Production of excess glucagon leads to conversion of glucose into glycogen. Whereas insulin signalling converts glycogen into glucose. Thus effects of excess glucagon can be counteracted by insulin