Cells of random sizes (some very small) are formed after cell division Normal sized cells are formed after cell division Cells do not divide, and turn into long filaments Cells die immediately upon shifting to 42°C
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Oogenesis
The formation of the ovum (mature female gamete) from undifferentiated germ cells is called oogenesis. This process takes place in the ovaries (female gonads). Oogenesis consists of three stages known as the multiplication phase, growth phase, and maturation phase.
Cell Division
Cell division involves the formation of new daughter cells from the parent cells. It is a part of the cell cycle that takes place in both prokaryotic and eukaryotic organisms. Cell division is required for three main reasons:
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- "Agent V" is the name of an anticancer (chemotherapy) drug. This drug works against cancer cells by inhibiting the formation of microtubules in sensitive cells. Consider a cell that is sensitive to agent V (in other words, agent V is effective at stopping growth of this cell). Based on this information, agent V would cause the cell to be frozen at which of the major cell cycle checkpoints (G1, G2 or M checkpoint)? ExplainA 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.What from mitosis is triggered by mitotic CDK inactivationmainly brought about by mitotic cyclin degradation.
- 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.Some cancer cells are insensitive to typical chemotherapy. Research into the mechanisms underlying this insensitivity uncovered an ability by these cells to pump the treatment drug out of the cell against its concentration gradient. Additional drugs have been developed that inhibit the pump, thus trapping the chemotherapeutic agent inside to promote cancer cell destruction. The Figure shows what happens when two types of cells are treated with a 3H-labeled anti-cancer drug, paclitaxel. Which set of cells (A or B) would be described as resistant to the cancer treatment? Explain your answer. What type of transport are the resistant cells using?Overexpression of the Myc protein is a common feature of many types of cancer cells, contributing to their excessive cell growth and proliferation. By contrast, when Myc is overexpressed in most normal cells, the result is not excessive proliferation, but cell-cycle arrest or apoptosis.Which one of the following statements provides the most likely explanation for why overexpression of Myc can have such different outcomes in normal cells and in cancer cells? A. Normal cells contain checks and balances that prevent Myc-induced proliferation. B. In normal cells, Myc protein acts as a mediator in cell-cycle arrest and apoptosis. C. The target protein for Myc-induced proliferation is missing from most normal cells. D. In normal cells, when Myc is overexpressed, the excess Myc protein precipitates.
- Cytokinesis in plant cells is different than cytokinesis in animal cells. a) Explain why it has to be different, andb) briefly describe the processes in the two different cell types.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.The p53 protein regulates the expression of BAX and Bcl2 to keep division at normal rate. Explain how is this achieved?
- The “Hayflick limit” is the number of times cells growing in tissue culture will divide before cell proliferation ceases. What experimental procedure can be employed to remove this limit?In other words, the master regulator initiates a program of gene expression that narrow the potential fates of the precursor's cells’ descendants to the type of cells that participate in the organ’s function. Question: Once a master regulator gene is turned on in some cells and not in others, how do cells “remember” that pattern through all the cell division that occur to form a specific organ?In normally dividing cells, once chromosomes have been properly segregated via the steps of mitosis, the two resulting “daughter cells” separate. In animal cells (and other cell types without a cell wall) the contractile ring plays a crucial role in the process of cytokinesis. Exactly how the contractile ring is accurately positioned, so as to be located midway between the two poles (ends) of the dividing cell, is still not fully understood, although factors released from the mitotic spindle are thought to play a role.Regardless of the precise positioning mechanism, one key player in the assembly of the contractile ring is the GTP/GDP binding protein Rho. In its active form, Rho can stimulate the activity of the actin-binding protein formin and (via effects on the myosin regulatory light chain) that of myosin II. Given their respective roles, why might activation of formin and myosin II be beneficial as cells assemble a functional contractile ring structure?