2005_Exam4_key_rev - Name_KEY 7.06 Cell Biology EXAM#4 This is an open book exam and you are allowed access to books a calculator and notes but not

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Name: ___________KEY_________________ 7.06 Cell Biology EXAM #4 May 18, 2005 This is an open book exam, and you are allowed access to books, a calculator, and notes but not computers or any other types of electronic devices. Please write your answers in pen (not pencil) to the questions in the space allotted. Please write only on the FRONT SIDE of each sheet. And be sure to put your name on each page in case they become separated! Remember that we will Xerox all of the exams. Good luck! Question 1. 18 pts __________ Question 2. 17 pts __________ Question 3. 30 pts __________ Question 4. 17 pts __________ Question 5. 18 pts __________
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Name: ___________KEY_________________ 10 min 20 min 30 min 40 min 10 min 20 min 30 min 40 min Question 1. (18 pts) DIRECTIONS: For each of the situations depicted in parts a) , b) , and c) , Name one example of a mutational event in a specific gene that would cause the defect shown in the data, AND… Discuss how this specific mutation explains mechanistically why the cells used in the experiment have been transformed into cancerous cells. (a, 6 pts) You perform the following experiment on normal cells and cancerous cells from a specific colon cancer. You incubate the cells with a short pulse of radioactive amino acids, and then chase for a long period of time with non-radioactive amino acids. You wait for different amounts of time during the chase, and immunoprecipitate β - catenin. You run the IPs on an SDS-PAGE gel and expose the gel to autoradiography film. The film you see is as follows, with the bands shown being β -catenin: There are many possible answers for which mutational event occurred in these cells. Acceptable answers include: a point mutation in beta-catenin so that it cannot be phosphorylated/degraded/inactivated, a deletion of GSK3 or APC or Axin so that beta- catenin cannot be inactivated, an over-supply of Wnt so that the Wnt pathway is always activated, a point mutation in the gene encoding the Wnt receptor (Frizzled) that causes the receptor to be hyperactive, or a point mutation in the gene encoding Dishevelled that causes Dishevelled to be hyperactive. (When Wnt binds to its receptor Frizzled, this causes Dishevelled to inactivate the GSK3/APC/Axin complex that normally inactivates beta- catenin.) NORMAL COLON CELLS CANCEROUS COLON CELLS
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Name: ___________KEY_________________ Any of these mutations would lead to the transformation of cells because each causes the Wnt pathway to send constitutive signaling, and the Wnt pathway leads to an output of cell growth and division. Beta-catenin is the transcription factor that turns on genes that promote cell growth. Beta-catenin is normally phosphorylated by GSK3 and thereby targeted for degradation, as shown by the short half-life of beta-catenin in wild-type cells. However, the stabilization of beta-catenin seen in the cancerous cells occurs because beta-
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This note was uploaded on 01/23/2012 for the course BIOLOGY lsm1301 taught by Professor Seow during the Spring '11 term at National University of Singapore.

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2005_Exam4_key_rev - Name_KEY 7.06 Cell Biology EXAM#4 This is an open book exam and you are allowed access to books a calculator and notes but not

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