Concept explainers
a.
To determine:
The type of cyclins (A, B, D, or E) to which SCF and APC couple ubiquitin.
Introduction:
The duplication of chromosomes and their accurate segregation into two daughter cells takes place during the cell cycle. The cell cycle is divided into four successive stages: G1, S, G2, and M. The cyclin-dependent kinases belong to a family of protein kinases that regulate the transition of the cell cycle from one stage to the next stage.
b.
To determine:
The method by which cells might activate SCF and APC only at the correct times.
Introduction:
The cyclin-dependent kinases function only after associating with proteins called cyclins. CDK-cyclin complexes can activate or deactivate target proteins by phosphorylation.
Want to see the full answer?
Check out a sample textbook solutionChapter 19 Solutions
Genetics: From Genes to Genomes, 5th edition
- See figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. A Explain what a kinase does and how the cyclin controls the activity of the Cdk.arrow_forwardSee figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. Cyclin Serine Lysine Aspartic "Acid Lysine -OH NH3t -Coo NH3+ NH3 + -OH Aspartic Aad Aspartic Acid /Lysine Serine сокarrow_forwardMutants of cyclin B that are resistant to degradation by the cyclin B protease have been generated. How would the presence of these cyclin B mutants affect the events at the metaphase to anaphase transition?arrow_forward
- What are the two main functions of the APC / cyclosome complex? Describe in detail.arrow_forwardWhich of the following is the most likely result of a mutation in the lac operator that prevents release of the depressor protein? Choose 1 answer: (A)The lactose permease protein will be produced, even in the absence of lactose. (B) Transcription of the structural genes will be blocked, even in the presence of lactose. (C) The catabolite activator protein will be bound to the CAP site, even in the presence of glucose. (D) Expression of the lacI gene will be repressed, even in the absence of glucose.arrow_forwardCell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.arrow_forward
- For each of the following situations, provide a plausible explanation for how it could lead to unrestricted cell division.(a) Colon cancer cells often contain mutations in the gene encoding the prostaglandin E2 receptor. PGE2 is a growth factor required for the division of cells in the gastrointestinal tract.(b) Kaposi sarcoma, a common tumor in people with untreated AIDS, is caused by a virus carrying a gene for a protein similar to the chemokine receptors CXCR1 and CXCR2. Chemokines are cell-specific growth factors.(c) Adenovirus, a tumor virus, carries a gene for the protein E1A, which binds to the retinoblastoma protein, pRb. (d) An important feature of many oncogenes and tumor suppressor genes is their celltype specificity. For example, mutations in the PGE2 receptor are not typically found in lung tumors. Explain this observation. (Note that PGE2 acts through a GPCR in the plasma membrane.)arrow_forwardAs a researcher who studies cytoskeletal dynamics, you create a microtubule subunit that cannot hydrolyze GTP. How would the critical concentration for the minus end of a polymer formed by these mutant subunits compare to that of the minus end of a fiber formed by normal microtubule subunits? Why? How would the critical concentration for the minus end of a fiber formed by these mutant subunits compare to that of the plus end of a fiber formed by normal microtubule subunits? Why?arrow_forwardYou are studying the M-cyclin. You treat mitotic cells with an inhibitor of the proteasome and find that M-cyclin is no longer degraded and that this prolongs mitosis. You also find that in the presence of the inhibitor, M-cyclin is now running slower/larger in a Western than you have previously doserved. In 1-2 sentences, explain why this might be happening.arrow_forward
- The 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.arrow_forwardIf you wanted to engineer the initiator caspase from the Fas/FasL extrinsic apoptosis pathway to function in the intrinsic pathway (e.g. in response to DNA damage), which of the following would be the most likely approach to succeed? O Replace the extrinsic pathway's initiator caspase Death Effector Domain with a CARD domain O Replace the Fas Death Domain with a cytochrome C binding domain O Generate a version of the Fas receptor that localizes to the mitochondrial intermembrane space 80 O Replace the intrinsic pathway's initiator caspase CARD domain with a Death Effector Domain F3 0 $ 4 DOD DOO R F4 S % 5 T No new data to save. Last checked at 3:01pm Submit Qu B4 ♫ 8 tv A F5 < 6 MacBook Air F6 Y & 7 F7 * 8 X F8 ( 9arrow_forwardOne form of anemia results when individuals have a deficiency in the enzyme phosphatidylinositol glycan A (PIGA). This enzyme is required for the membrane attachment of proteins anchored by glycolipids to the plasma membrane, using what is called a ‘GPI-linkage.’ Included in the group of GPI-linked cell surface proteins is DAF/CD55. These individuals become anemic because: DAF/CD55 prevents the lysis of red blood cells by infecting pathogens. DAF/CD55 normally prevents the spleen from clearing healthy red blood cells from the circulation. In the absence of PIGA, the red blood cell membrane is bare of proteins allowing increased access of complement activating proteins to attach to the cell membrane. DAF/CD55 is a complement inhibitory protein that inactivates any C3 convertase that may form on host cell surfaces. In the absence of PIGA, red blood cells are unable to synthesize high levels of hemoglobin.arrow_forward
- Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
- Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & CompanyLaboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education