A second hit might also occur through loss of heterozygosity (LOH). An example of how LOH may occur by reciprocal crossing over during mitosis is diagrammed in the figure attached. Discuss and interpret this model. Write a brief explanation of (a) what LOH means and (b) how LOH by mitotic reciprocal crossing over can give rise to a cell lineage with functional loss of the wild-type copy of a tumor suppressor gene.

When the gene encoding a certain cellular kinase is deleted, the resulting mutant cells arrest in the cell cycle and do not divide. These mutants can be rescued when a gene encoding an N-terminal GFP fusion of the protein is expressed, but not when a gene encoding a C-terminal GFP fusion is expressed. Which fusion protein is appropriate to use in studying cellular localization and activity? Explain why.

There is a protein called neurogenin that stimulates neuronal cells to differentiate. In order to determine what kind of receptor neurogenin binds to, you add a general phosphatase (one that can remove phosphates from any substrate) to neural cells when you add neurogenin, and you discover that this inhibits differentiation. Furthermore, in the presence of this phosphatase, you find that not even a G protein is activated in response to neurogenin. 1.  With this information, what kind of receptor does neurogenin bind to? 2.  In a normal cell, how does the G protein in this pathway get activated? 3.  In a normal cell, why does the response to neurogenin cease over time?

Is the following true or false AND EXPLAIN: Cells with one functional copy of a proto-oncogene will usually proliferate faster than normal cells.

In cell growth, how does the normal allele of BRCA1 work? Is it an oncogene or a tumor suppressor gene?

List and describe 4 of the main regulators of the cell cycle. Then describe the involvement of a CDK substrate at each stage of the cell cycle: G1, S, G2, M. 2. DESCRIBE (do not just list) three mechanisms that keep the cell cycle moving in only one direction. Then describe how these mechanisms play a role at one specific stage of the cell cycle. 3. What are the three main classes of genes implicated in cancer? Describe each one and give an example of each one. 4. DESCRIBE (do not just list) 4 developmental strategies that cause different cells and tissues to acquire different identities during embryogenesis. Then explain how iPS cells are an exception to the overall trend of cells decreasing in pluripotency as they develop. 5. Describe three unique cell biological features of sperm cells and three unique cell biological features of egg cells. By "unique", I mean a feature that is not common in most cells. 6. You have just identified a mouse gene that is homologous to other vertebrate…

Recall that the nuclear membrane disintegrates late in prophase of mitosis in most eukarvotic cells. Once the membrane is reformed in telophase in a daughter cell, several components of gene expression mignt therefore be "caught" out in the cytoplasm when they would otherwise onlv ever be found inside the nucleus. Consider where the following components of gene expression are made and where they runction. Which component is normally never found in the cytoplasm outside the nucleus? O A. Spliced intron • B. RNA polymerase O C. Histones • D. DNA polymerase

What is the most likely outcome is we lose the tumor suppressor proteins, cyclin- dependent kinase inhibitors. Select one: o a. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will not proceed. o b. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will not proceed. o c. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will proceed. o d. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will proceed.