Biological Science (7th Edition)
7th Edition
ISBN: 9780134678320
Author: Scott Freeman, Kim Quillin, Lizabeth Allison, Michael Black, Greg Podgorski, Emily Taylor, Jeff Carmichael
Publisher: PEARSON
expand_more
expand_more
format_list_bulleted
Concept explainers
Textbook Question
Chapter 12, Problem 15PIAT
In normal cells, stathmin is inactivated by phosphorylation at the start of M phase. Phosphatases remove these phosphates as the cell transitions from M phase to G1. What enzyme is likely to be responsible for phosphorylating stathmin during M phase?
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solutionStudents have asked these similar questions
Stathmin is phosphorylated by cyclin dependent kinases in response to extracellular signals such as growth factors. To further understand the role of phosphorylation in stathmin function, you decide to
treat cells with growth factors in the presence or absence of phosphatase and observe microtubule dynamics. Based on the known function of stathmin, and phosphorylation of stathmin, how would you
expect phosphatase treatment to affect microtubule dynamics?
A. Decreased frequency of catastrophe in the presence of phosphatase, compared to untreated control
B. Increased frequency of catastrophe in the presence of phosphatase, compared to untreated control
C. Rapid microtubule polymerization in the presence of phosphatase, compared to untreated control
D. Catastrophe frequency is the same in phosphatase treated and control cells
Which of the following changes to the microtubule binding protein, Tau, commonly occurs in Alzheimerâ s and other neurodegenerative diseases?
A
Tau is hypo-phosphorylated and does not bind to microtubules to destabilize them.
B
Tau levels are so low in the cell that they only bind to some microtubules.
C
Tau is hyper-phosphorylated and does not bind to microtubules to stabilize them.
D
Microtubules are hyper-phosphorylated and do not bind to Tau.
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 active
Chapter 12 Solutions
Biological Science (7th Edition)
Ch. 12 - 1. Which statement about the daughter cells...Ch. 12 - After S phase, what comprises a single chromosome?...Ch. 12 - Progression through the cell cycle is regulated by...Ch. 12 - 4. What major events occur during anaphase of...Ch. 12 - 5. Identify at least two events in the cell cycle...Ch. 12 - 6. What evidence suggests that during anaphase,...Ch. 12 - 7. Evaluate each of the following defects. Which...Ch. 12 - Prob. 8TYUCh. 12 - Prob. 9TYPSSCh. 12 - Prob. 10TYPSS
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- 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.arrow_forwardMost mammalian cells have a single immobile cilium called the primary cilium, in which intraflagellar transport (IFT) motor proteins move elements of the Hedgehog (Hh) signaling pathway along microtubules. What parts of the Hh signaling pathway would mutations in the IFT motor proteins Kif3A, Kif7, and dynein disrupt?arrow_forwardMany common medications function by interrupting the normal operation of certain signal transduction pathways. Which of the following describes a possible mechanism by which a certain medication may interrupt a signal transduction pathway? A A medication enters the target cell and triggers apoptosis by causing the release of di- gestive enzymes from cell lysosomes. B A medication interacts with the phospholipid bi-layer of the cell membrane and in- creases its permeability. с D A medication binds to membrane-bound glucose proteins and acts as an allosteric in- hibitor that prevents the intake of glucose by the cell. A medication diffuses through the membrane of a target cell and inhibits an enzyme that normally synthesizes a second messenger.arrow_forward
- When a clam sperm contacts a clam egg, it triggers ionic changes that result in the breakdown of the egg nuclear envelope, condensation of chromosomes and initiation of meiosis. Two observations confirm that ionic changes initiate these cellular events: suspending clam eggs in seawater containing 60 mM KCl triggers the same intracellular changes as do sperm suspending eggs in artificial seawater lacking calcium prevents activation by 60mM KCl. The intracellular K+ concentration is 344mM and that of normal seawater is 9 mM. Why does 60mM KCl affect the changes mimicking the sperm cell? please explain. What does the lack of activation by 60mM KCl in calcium-free seawater suggest about the mechanism of KCl activation? please explain the mechanism.arrow_forwardVery briefly, explain how increased cytoplasmic IP3 levels can then increase cytoplasmic calcium (Ca2+) levels.arrow_forwardThe 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_forward
- Select the most accurate explanation for how vesicular transport occurs when a receptor is moving from the plasma memberane to the late endosome/lysosome. A. Endosomes containing the receptor are transported by myosin II walking towards the minus end of microtubules. Endosomes are targeted to the late endosome/lysosome by Rab and SNARES facilitate membrane fusion. B. Endosomes containing the receptor are transported by myosin V walking towards the minus end of microtubules. Endosomes are targeted to the late endosome/lysosome by Rab and SNARES facilitate membrane fusion. OC. Endosomes containing the receptor are transported by dyenin walking towards the minus end of microtubules. Endosomes are targeted to the late endosome/lysosome by Rab and SNARES facilitate membrane fusion. D. Endosomes containing the receptor are transported by kinesin-13 walking towards the plus end of microtubules. Endosomes are targeted to the late endosome/lysosome by clathrin and SNARES facilitate membrane…arrow_forward"given the numerous processes inside cells that are regulated by changes in Ca+2 concentration, it seems likely that Ca¹²-dependent cell-cell adhesions are also regulated by changes in Ca2 concentration" is true or false.arrow_forwardAfter 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.arrow_forward
- To design a drug that inhibits metastasis, which of the following strategies is the WORST idea? to disrupt cadherin complexes to inhibit Rho family proteins to inhibit ARP complex O to block myosin-based contractile structurearrow_forwardA rise in the intracellular Ca2+ concentration causes muscle cells to contract. in addition to an ATP- driven Ca2+ pump, muscle cells that contract quickly and regularly, such as those of the heart, have an additional type of Ca2+ pump—an antiport that exchanges Ca2+ for extracellular Na+ across the plasma membrane. The majority of the Ca2+ ions that have entered the cell during contraction are rapidly pumped back out of the cell by this antiport, thus allowing the cell to relax. ouabain and digitalis are used for treating patients with heart disease because they make heart muscle cells contract more strongly. both drugs function by partially inhibiting the Na+ pump in the plasma membrane of these cells. can you propose an explanation for the effects of the drugs in the patients? What will happen if too much of either drug is taken?arrow_forwardCystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR (cystic fibrosis transmembrane-conductance regulator) gene, which encodes the CFTR protein. The cells of the lining of the lungs contain high levels of the CFTR protein in their membranes. Normally, CFTR contains a chloride ion channel, which permits chloride ions to pass from inside the cells to the cells’ surfaces. The surface chloride ions are able to attract water in the lungs, allowing for the formation of a water layer on the cells’ surfaces. This thin water layer is necessary to allow the cilia, the tiny hairs on the surface of the lining cells to move back and forth easily. This motion permits the removal of mucus from the lungs. A particular error in the CFTR gene results in the replacement of the amino acid Phe with Ser at residue 508 of the CFTR protein. Individuals afflicted with CF most often experience the presence of thick, dry and sticky mucus in the lungs, leading to chronic infections and…arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- 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
Human Anatomy & Physiology (11th Edition)
Biology
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:PEARSON
Biology 2e
Biology
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:OpenStax
Anatomy & Physiology
Biology
ISBN:9781259398629
Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa Stouter
Publisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)
Biology
ISBN:9780815344322
Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter
Publisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & Physiology
Biology
ISBN:9781260159363
Author:Martin, Terry R., Prentice-craver, Cynthia
Publisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)
Biology
ISBN:9781260231700
Author:Sylvia S. Mader, Michael Windelspecht
Publisher:McGraw Hill Education
The Cell Cycle and its Regulation; Author: Professor Dave Explains;https://www.youtube.com/watch?v=eqJqhA8HSJ0;License: Standard YouTube License, CC-BY
Cell Division - Mitosis and Meiosis - GCSE Biology (9-1); Author: Mr Exham Biology;https://www.youtube.com/watch?v=w7vp_uRA8kw;License: Standard YouTube License, CC-BY