ANAT 365 Study Guide - Peroxidase, Cell Membrane, Transmembrane Protein
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The mechanism of dynamin activity is not fully understood. Thereare two schools of thought on the matter. The first one suggeststhat the GTPase activity of dynamin allows dynamin to pinch off theneck of the vesicle. The other suggests that the GTP-bound form ofdynamin acts as a signal to recruit other enzymes that actually dothe pinching of the membrane. Since you are a cell biology stud,you decide to do an experiment to answer this questiononce-and-for-all. To do this, you prepare a mutated form of thedynamin gene that prevents it from hydrolyzing its bound GTP. Youthen perform an experiment where you express the mutated dynamingene, along with the proper controls, in animal cells lacking afunctional, endogenous dynamin gene and analyze the ability ofthose cells to form clathrin-coated vesicles. Answer the followingquestions using the data when necessary.
Cells expressing... | Result |
wild-type dynamin | + |
mutant dynamin | + |
no dynamin | - |
A. In what state is the mutant dynamin – active or inactive? In2-3 sentences, explain why you chose that answer.
B. Which of the two schools of thought does the data support?USE THE DATA GIVEN to explain your answer in 2-3 sentences.
C. What would the data look like if the other school of thoughtwas supported? Explain why in 2-3 sentences.
Based on your success with “fakeprotein” kidney disease, you start looking at other illnesses linked to the FP gene. It turns out that while there are no other human diseases known to be linked to it, there is a disease called Krazy Koala Syndrome and the KKS gene turns out to be very similar to FP in humans. The afflicted Koala’s jump out of trees and attack the much larger animals for no reason, dying very young. When the brains of these Koala;s are evaluated, the have the spongiform character of Mad Cow Disease brains. This is typically caused by aggregates of the protein forming. Like before, there are normal KKS/FP proteins in other tissues. The KKS pre-mRNA looks like this:
Ca2+ bind dimerization Protease
Exon | Intron | Exon | Intron | Exon |
The dark blocks are exons and the light blocks are introns. In normal Koala’s, you find only the full length protein (all 3 exons) in most cells, but in neurons you only find the 1st and 2nd exons. In KKS Koala’s you find a mix of the two proteins in neurons, but only the full length everywhere else.
A. There are two possible ways that alternative splicing can result in the formation of these two isoforms. What are they? What does each predict about the mutation that might be responsible for the phenotype?
B. Give an example of an experiment to test for one of these explanations. Describe what result would support the hypothesis.