Blog

Use context clues to fill in the blanks (Position 1 refers to the first blank, etc.) with the most appropriate terms for the sentence to have meaning as a whole. Each term will only be used once or not at all.    Our home, _____1_____, is orbiting around the ____2______, the only such object in our ____3______, which is one such object orbiting in the _____4_____, one such object orbiting in the _____5_____, which is one such collection orbiting in the ______6____.

Where would all visible stars be circumpolar? 

The following schematic diagram shows the activation of M-Cdk in mitosis. Indicate which proteins below correspond to those indicated as A to D in the diagram. Your answer would be a four-letter string. (  ) Wee1 (  ) CAK (  ) Cdc25 (  ) M-cyclin

Activated protein kinase C (PKC) can lead to the modification of the membrane lipids in the vicinity of the active PKC. The Figure below shows how G proteins can indirectly activate PKC. You have discovered the enzyme activated by PKC that mediates the lipid modification. You call the enzyme Rafty and demonstrate that activated PKC directly phosphorylates Rafty, activating it to modify the plasma membrane lipids in the vicinity of the cell where PKC is active; these lipid modifications can be detected by dyes that bind to the modified lipids. Cells lacking Rafty do not have these modifications, even when PKC is active. Which of the following conditions would lead to signal-independent modification of the membrane lipids?    

Indicate whether each of the following mutations would likely promote (P) or inhibit (I) apoptosis in cells harboring the mutation(s). Your answer would be a four-letter string composed of letters P and I only, e.g. PPPI. (  ) Mutations in the pro-apoptotic effector Bcl2 family proteins Bax and Bak that prevent their association with the outer mitochondrial membrane. (  ) A mutation in the BIR domain of the IAP protein DIAP1 that prevents binding to either caspases or anti-IAP proteins. (  ) A mutation in the anti-IAP protein Reaper that prevents its binding to the IAP proteins. (  ) A mutation in the CARD domain of caspase-9 that prevents its binding to Apaf1.

In the presence of an ATP analog that can bind myosin normally but cannot be hydrolyzed…

You have created a green fluorescent protein (GFP) fusion to a protein that is normally secreted from yeast cells. Because you have learned about the use of temperature-sensitive mutations in yeast to study protein and vesicle transport, you obtain three mutant yeast strains, each defective in some aspect of the protein secretory process. Being a good scientist, you of course also obtain a wild-type control strain. You decide to examine the fate of your GFP fusion protein in these various yeast strains and engineer the mutant strains to express your GFP fusion protein. However, in your excitement to do the experiment, you realize that you did not label any of the mutant yeast strains and no longer know which strain is defective in what process. You end up numbering your strains with the letters A through D, and then you carry out the experiment anyway, obtaining the results shown in Figure below (the black dots represent your GFP fusion protein). Name the protein that is defective in each of these strains. Remember that one of these strains is your wild-type control.

The following happens when a G-protein-coupled receptor activates a G protein.  

You have isolated a mutant in which a fraction of the new cells die soon after cell division, and a fraction of the living cells have an extra copy of one or more chromosomes. When you grow the cells under conditions where they transit the cell cycle more slowly, the defect disappears, suggesting that the mitotic spindle and segregation machinery are normal. 1) What checkpoint may be defective in the cell cycle of the mutant? Explain your reasoning. 2) Describe in great detail the normal operation of such checkpoint.

a) Describe the checkpoint involving Rb. b) What is the phenotype of a mutant cell lacking Rb? c) What about a cell overexpressing Rb?