What is the effect of having fluctuating cyclin levels throughout the cell cycle, while the levels of its corresponding cyclin dependent kinase stay relatively constant? Explain.
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What is the effect of having fluctuating cyclin levels throughout the cell cycle, while the levels of its corresponding cyclin dependent kinase stay relatively constant? Explain.
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- Why doesn't Cdk1 active immediately upon binding to cyclin B? What other components of the cell’s regulatory machinery could explain the delay in activation of the kinase activity?The destruction of the various cyclins is commonly used to inactivate the Cdk/cyclin complexes. Why is it advantageous to inactivate these complexes via protein destruction instead of some other method that does not require the re-synthesis of a cyclin protein the next time the cell divides?Cyclin-dependent kinases are a type of "microchip" protein that require multiple inputs (i.e., structural alterations) to be activated-- and thus are active only under specific conditions (as shown in the diagram below). How does limiting activity to when all conditions have been met help the cell function properly? INPUTS has this phosphate been removed? been added? has this is cyclin present? phosphate
- Which of the following is false about cyclin-cdk complexes? OCdk's do not have to bind to cyclin proteins for complex to be active. OCdk/cyclin complexes phosphorylates proteins required to trigger next cell cycle phase. Process acts as molecular brakes to ensure cell is ready to continue with cell cycle. O Cyclin concentrations increase gradually, but cdk must be phosphorylated by specific kinase for complex to be activeNotch signaling orchestrates transition from G1 to S phase of cell cycle by multiple other interactions that target the G1/S checkpoint machinery. This is a highly conserved pathway that is seen across multiple kingdoms of life and the ligands involved in notch signaling are typically membrane-bound proteins. This suggests that: -This pathway relies on hormone interactions via endocrine pathways -This pathway relies on signal propagation via paracrine molecules -This pathway relies on direct signaling across gap junctions -This pathway relies on cell binding via autocrine signalingThe small, monomeric protein Rho has acquired a mutation by which it is constitutively activated and evenly distributed along with the cytoplasmic leaflet of the plasma membrane. Describe the effects this would have on cell crawling. A complete answer will include a description of normal Rho distribution and activation, an explanation of Rho function in cell crawling, and a thoughtful argument for an overall effect of the mutation on cell crawling that is based on the specific roles of Rho.
- RAS is a signal transducer that acts as a switch for turning on cell division. Drag the descriptions below to their proper places on the figure to show the sequence of events. When growth factor binds to the receptor, the intracellular domain activates RAS by facilitating exchange of GDP for GTP. When no growth factor is bound to the extracellular receptor, RAS is bound to GDP and is inactive. RAS activates the first of three sequential kinase proteins termed the MAP kinase cascade. Cell proliferation proceeds as the machinery for cell division is set in motion. The end result of the MAP kinase cascade is activation of a transcription factor. Receptor 1 Ras GDP 2 4 5 Growth factor Ras GTPAfter a cell "clears" the G₁ restriction checkpoint, it can proceed into S phase. This S phase entry is achieved by a cyclin dependent kinase (Cdk2) and its cyclin (Cyclin E), but additionally requires the action of a protein kinase (CDC2) as well as a phosphatase (CDC25) enzyme. Explain how these 4 proteins work together to orchestrate S phase entry.A temperature-sensitive mutant yeast strain stops dividing when shifted from 25°C to 37°C. These cells are analyzed at different temperatures by a machine that measures the amount of DNA they contain, and the following graphs are obtained. number of cells number of cells [ Select] [Select] [Select] 25°C [Select] مل Cells in G1 phase should have [Select] Which of the following would explain the behavior of your mutant? Mark yes or no for each of the following choices. 2 amount of DNA/cell (arbitrary units) 37°C 1 2 amount of DNA/cell (arbitrary units) unit(s) amount of DNA. ✓ Inability to initiate DNA replication Defect in chromosome condensation ✓Defect in centrosome duplication ✓Defect in cytokinesis
- You are studying three proteins that you think are important Yor progression through the cell cycle. You know that one of them is a phosphatase (P1) and the other two are kinases ( K1 and K2). You add these enzymes in different combinations as shown below, and find that they have different effects on the activity of a cyclin dependent kinase, cdk2p. cdk2p Inactive Active cdk2p + K1 cdk2p + K2 Inactive cdk2p + K1 + K2 Inactive cdk2p + P1 cdk2p + P1 + K2 cdk2p + P1 + K1 Inactive Inactive Active cdk2p + P1 + K1 + K2 ActiveIn Xenopus, one of the substrates of mitotic CDKs is the phosphatase Cdc25. When phosphorylated by mitotic CDKs, Cdc25 is activated. What is the substrate of Cdc25? How does this information help to explain the rapid rise in mitotic CDK activity as cells enter mitosis?Describe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.