Biology 3316A/B Lecture Notes - Lecture 16: Mst1, Cilium, Primary Cell

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teallion850

25 Mar 2019

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Hippo/mst1: hippo is to flies as the mammalian sterile is to us, hippo pathway is a kinase cascade, one needs to activate one in order to activate the next one, etc. All of these enzymes are sitting dormant, not doing anything, until their activation. Fly discovered that if you mutate hippo gene, there is uncontrolled cell growth. Cell density dictates whether you have an activate pathway or not: mst1 overexpression doesn"t do a proliferative effect. If you turn the overexpression off, that is when the liver goes back to normal size. Cell density dictates whether you have an active pathway or not. Signature for 14-3-3 to come along and keep it out of the nucleus. Cell density gets too high stop proliferation. If you don"t cells continue to proliferate and then they get to about 1 million cells and have to proliferate, otherwise, the internal part of the tumour will die. The livers don"t have the same number of cells!

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Given the scenario/situation, respond to all questions with complete sentences.

Scientists have been studying the effects of Starkagaren Disease, which is regulated by the stgn gene, in cultured normal and breast cancer cell lines. They have fused a yellow fluorescent probe to the end of the stgn gene to study the disease more closely. By adding a probe, it will create a hybrid protein that emits a yellow color under a blue laser. This hybrid protein is known as a fluorescentâtagged protein, meaning that the protein itself will function and fold normally but it will be tagged with a yellow fluorescent probe (YFP) at the end. This allows the scientists to follow the protein through the cell cycle. They find that the stgn protein normally binds to centromeres in normal cells. After looking at cells at various stages of the cell cycle, they find that compared to normal cells, the breast cancer cells that express the Starkagaren Disease display abnormal nuclei, some appear very large, some have tiny nuclei, and some cells do not have a nucleus at all.

a) Because the STGN protein binds to the centromere, the scientists can also study what other structure?

b) After looking the defects of the affected cells, where in the cell cycle would you guess the error occurs? What do you think happens?

c) The stgn gene appears to not be functioning, do you think the scientists are able to see the STGN protein at the centromeres? Why?

d) The scientists want to see what would happen if they could block the stgn gene from being made in normal cells or lung cancer cells, what is one way they could do this?

rosecockroach918

{Reposted Question} Given the scenario/situation, respond to all questions with complete sentences.

Scientists have been studying the effects of Starkagaren Disease, which is regulated by the stgn gene, in cultured normal and breast cancer cell lines. They have fused a yellow fluorescent probe to the end of thestgn gene to study the disease more closely. By adding a probe, it will create a hybrid protein that emits a yellow color under a blue laser. This hybrid protein is known as a fluorescentâtagged protein, meaning that the protein itself will function and fold normally but it will be tagged with a yellow fluorescent probe (YFP) at the end. This allows the scientists to follow the protein through the cell cycle. They find that the stgn protein normally binds to centromeres in normal cells. After looking at cells at various stages of the cell cycle, they find that compared to normal cells, the breast cancer cells that express the Starkagaren Disease display abnormal nuclei, some appear very large, some have tiny nuclei, and some cells do not have a nucleus at all.

a) Because the STGN protein binds to the centromere, the scientists can also study what other structure?

b) After looking the defects of the affected cells, where in the cell cycle would you guess the error occurs? What do you think happens?

c) The stgn gene appears to not be functioning, do you think the scientists are able to see the STGN protein at the centromeres? Why?

d) The scientists want to see what would happen if they could block the stgn gene from being made in normal cells or lung cancer cells, what is one way they could do this?

copperferret659

1.In 1971, Dr. Judah Folkman published the âangiogenic hypothesisâ suggesting that a tumor cannot grow beyond 1â2 millimeters without the development of new blood vessels (angiogenesis) that provide access to oxygen and nutrients. During the 1990s, it was discovered that vascular endothelial growth factor (VEGF) stimulates migration and proliferation of the cells that form blood vessels, leading to the formation of new blood vessels. VEGF binds to receptor tyrosine kinases (RTKs) on the cell surface and causes the RTKs to dimerize and become active, thereby initiating an intracellular signaling cascade that stimulates cell division and inhibits apoptosis. Many cancer cells secrete high levels of VEGF and increased VEGF expression in a tumor is correlated with a poor medical outcome for the patient. You work for a biotechnology company that seeks to create anti-cancer drugs that prevent growth of tumors and/or cause tumors to shrink, while leaving normal cells relatively untouched. Your company has purchased the rights to therapeutic uses of VEGF derived proteins as anti-tumor drugs. You have found that the VEGF protein has 2 domains, one involved in receptor binding, the other is required for dimerization of VEGF. You propose to make mutant versions of the protein that will act as antagonists of the receptor to be given to patients as an IV treatment as a way to inhibit the endogenous VEGF secreted by the tumor.

a.Which of the 2 domains should you mutate (receptor binding or dimerization)?

b. How do you expect the introduction of the mutant protein into the bloodstream of patients to block tumor progression (in other words, why did you change the domain in part a)?

peachmoose600

Biology 3316A/B Lecture Notes - Lecture 16: Mst1, Cilium, Primary Cell

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