You are studying Protein X which plays a role in promoting the G1/S phase transition in eukaryotic cells. You design an experiment using wild-type yeast cells to measure the amount of Gene X MRNA and activity levels of Protein X during the cell cycle. The results from your experiment are shown in the graph below. From the data, which of the following would most likely result from increased activity of Protein X? Select all that apply - Protein X activity levels Gene X MRNA levels Relative Units G1 G2 M Activation of the anaphase promoting complex (APC/C) and cleavage of cohesin proteins Activation of proteins that bind to Ori (origin of replication) sites Increased levels of dynamic instability of microtubules O Increased phosphorylation of nuclear lamin proteins, leading to breakdown of nuclear lamina structure
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- A researcher studying a line of cancer cells noticed that cellular content of RhoBTB3 and Cyclin E1 increase and decrease through the cell cycle. a. He hypothesizes that RhoBTB3 signaling regulates the production of Cyclin E1 and the entry of the cell into mitosis. Based on the data below, explain why his results do not support this hypothesis. Identify what conclusions are supported by this data. b. Suppose that the researcher can engineer a cell line in which RhoBTB3 expression can be induced by the addition of a drug. Design an experiment using this cell line to test whether RhoBTB3 regulates the production of Cyclin E1. Describe what results he can expect if his hypothesis is correct.Aurora AAurora A is a protein that acts as a kinase (transfers phosphates to molecules). Many types of cancer cells, including breast cancer cells, have higher than normal levels of this protein.Expressions of Aurora A genes in normal breast tissues (n = 10), normal tissues adjacent to tumors (n = 12) and breast tumors (n = 14).Scientists studying the production of Aurora A protein in normal frog cells observed that the amount of this protein in the cells changed throughout the cell cycle.Scientists tested chemicals that block Aurora 2 to see if they could be used as anti-cancer drugs. They found that some of the candidate drugs did slow the growth of cancer cells in cell culture in the lab. But when they tested these drugs in cancer patients to see if the drugs could slow the growth of solid tumors, they found that the benefit to patients was small when compared to the development of severe side effects such as anemia (low red blood cell count) and leukopenia (low white blood cell…Which of the following statements is a lie?Select one: a. If damaged DNA is detected during the cell cycle, negative regulation is responsible in stopping the cell cycle. b. There are four cyclin proteins involved in the positive regulation of the cell cycle and they have fluctuating levels. c. To activate cyclin-dependent kinases (Cdks), they must bind to another kinase.
- You are researching the regulation of cell-size control and discover that a signaling pathway that acts through a particular enzyme-coupled receptor is important for the size growth (enlargement) of rat kidney cells. Receptor activation causes activation of adenylyl cyclase, which ultimately leads to the activation of PKA. PKA then phosphorylates a transcription factor called BTS on threonine 84. This phosphorylation is required to allow BTS to bind to specific regulatory DNA sequences, increasing the transcription of Zrt2, a gene encoding a protein vital for kidney cell growth. You find that kidney cells without this receptor are 25% smaller than normal cells. When you measure cells expressing a constitutively active version of PKA, you find they are 25% bigger than normal kidney cells. Based on these results, predict whether a kidney cell’s size would be bigger or smaller than normal kidney cells in each of the following circumstances. Explain why in 1-2 sentences for each. You…You are researching the regulation of cell-size control and discover that a signaling pathway that acts through a particular enzyme-coupled receptor is important for the size growth (enlargement) of rat kidney cells. Receptor activation causes activation of adenylyl cyclase, which ultimately leads to the activation of PKA. PKA then phosphorylates a transcription factor called BTS on threonine 84. This phosphorylation is required to allow BTS to bind to specific regulatory DNA sequences, increasing the transcription of Zrt2, a gene encoding a protein vital for kidney cell growth. You find that kidney cells without this receptor are 25% smaller than normal cells. When you measure cells expressing a constitutively active version of PKA, you find they are 25% bigger than normal kidney cells. Based on these results, predict whether a kidney cell’s size would be bigger or smaller than normal kidney cells in each of the following circumstances. Explain why in 1-2 sentences for each. You add…Regulation of the cell cycle is very complex and involves multiple proteins. In yeast, a complex of cdc2 and a mitotic cyclin is responsible for moving the cell past the G2/M checkpoint. The activity of the cyclin-dependent kinase cdc2 is inhibited when it is phosphorylated by the kinase, Wee-1. What would you predict would be the phenotype of a Wee-1 mutant yeast? What other genes could be altered in a Wee-1 deficient mutant strain that would make the cells act normally?
- A Patients with an inherited cancer have a mutation in a zinc-finger motif of P21 (a cell-cycle regulatory gene). Which of the following is the most likely result of this A) Decreased binding of a transcription factor to a DNA sequence B) Enhanced binding of hormones to receptors C) Enhanced transport of a hormone receptor complex into the nucleus D) Stimulation of mRNA synthesis E) "Unzipping" of leucine-rich helicesYeast chromosome XII contains the HAP1 gene that contains codes to regulate proteins involved with cellular division. The SCM4 gene, on chromosome VII, produces membrane proteins and has a binding site for HAP1 in its promoter region. The diagram shows the location of the binding site for HAP1. Which of the following claims could scientists make regarding the interaction between HAP1 and SCM4? A - HAP1 would prevent translation of all SCM4 proteins by blocking the binding sections of messenger RNA and amino acids. B - HAP1 would decrease the translation of SCM4 proteins because promoter sections first bind transfer RNA and amino acids. C - HAP1 would stimulate transcription factors such as RNA polymerase and prevent all SCM4 proteins from beginning transcription. D - HAP1 would increase the transcription of SCM4 proteins because promoter sections bind RNA polymerase and initiate transcription.Explain why we can say that M-phase of the cell-cycle is triggered by a positive feedback loop. a) What would the consequences be if cohesins were working normally but condensins were not? and b) what stage of the cell cycle would this cause problems in? Why is it important for the centrosome to duplicate during G1-G2 (interphase) before M phase? The kinetochores serve as a link between the sister chromatids and the microtubules attached to the mitotic spindle. a) How are microtubules still able to exhibit dynamic instability after they are bound to the sister chromatids and b) why is this important to mitosis? As the name suggests, the Anaphase-promoting-complex (APC), promotes the 4th phase of mitosis by separating the sister chromatids so they can travel to separate poles of the cell, and prevents them from being re-zipped together. Describe how APC does these two things (Hint: one involves M-cyclin and the other involves…
- A small amount if cytoplasm isolated from a mitotic cell is injected into an unfertilized frog oocyte, causing the oocyte to enter M phase. A sample of the injected cytoplasm is then taken and injected into a second oocyte, causing this cell also to enter the M phase. this process is repeated many times until essentially, none of the original protein samples remains, and yet, cytoplasm taken from the last in the series on injected oocytes is still able to trigger entry into the M phase with undiminished efficiency. Explain this remarkable observation.Biologists have long been interested in the effects of radiation on cells. In one experiment, researchers examined the effect of radium on mitosis of chick embryo cells growing in culture. A population of experimental cells was examined under the microscope for the number of cells in telophase (as a measure of mitosis occurring) before, during, and after exposure to radium. The results are shown in the Figure. What is the effect of radium exposure on mitosis? Source: R. G. Canti and M. Donaldson. 1926. The effect of radium on mitosis in vitro. Proceedings of the Royal Society of London, Series B, Containing Papers of a Biological Character 100:413419.After the initial Actualization of the Cit+ phenotype, there was another alteration to the A-3 genome that resulted in increased growth (e.g. Refinement). What explained the increase in growth rate in response to Refinement? A. Increase number of transporters localized to the plasma membrane. B. Increased ability to metabolize glucose. C. Increased citric acid cycle activity. D. Altered promoter activity resulting in constitutive gene expression.