Loose Leaf For Integrated Principles Of Zoology
18th Edition
ISBN: 9781260411140
Author: Cleveland P Hickman Jr. Emeritus, Susan L. Keen, David J Eisenhour Professor PhD, Allan Larson, Helen I'Anson Associate Professor of Biology
Publisher: McGraw-Hill Education
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Chapter 3, Problem 1FFT
Summary Introduction
To propose: The reasons why the CFTR channel may not be present in the plasma membrane of some cystic fibrosis patients or may not function correctly in other patients.
Introduction: Cystic fibrosis is the inherited genetic autosomal recessive disorder. It is caused by the mutation in the gene that codes for transmembrane protein channel and that allows for the movement of chloride ions. As a result of this, the body produces thick and sticky mucus that obstructs the lungs.
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Cystic 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…
A genetic mutation leads to reduced function/loss of function of the V-ATPase on the surface of cellular lysosomes. Explain the role of the V-ATPase on the lysosomal membrane and the possible consequences of the reduced/lost function of this membrane protein.
Cystic fibrosis (CF) is a disorder caused by a random change in the gene that produces the
cystic fibrosis transmembrane conductance regulator (CFTR) protein. In people with CF,
random CFTR gene changes can disrupt the CFTR protein's normal production or function-
ing. This protein is typically found in several organs, and as a result, the lungs, pancreas, di-
gestive system, and other organs are affected. The symptoms of CF can range from breath-
ing difficulties to recurrent infections.
Which of the following best describes the effects of cystic fibrosis?
A
B
с
D
Cystic fibrosis is caused by a gene with multiple alleles.
Cystic fibrosis is inherited via incomplete dominance.
Cystic fibrosis is a pleiotropic gene.
Cystic fibrosis is caused due to polygenic inheritance.
Chapter 3 Solutions
Loose Leaf For Integrated Principles Of Zoology
Ch. 3 - Prob. 1RQCh. 3 - Briefly describe the structure and function of...Ch. 3 - Name two functions each for actin and tubulin.Ch. 3 - Prob. 4RQCh. 3 - What are the functions of each of the main...Ch. 3 - Our current concept of the plasma membrane is...Ch. 3 - The plasma membrane is an effective barrier to...Ch. 3 - You place some red blood cells in a solution and...Ch. 3 - Distinguish among phagocytosis, pinocytosis,...Ch. 3 - Define the following: chromosome, centromere,...
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- Microtubules are important for transporting cargo in nerve cell axons, as diagrammed in Figure Q17- 33. Notice that the two types of cargo are traveling in opposite directions. Which of the following statements is likely to be false? cell body microtubule axon Figure Q17-33 inward transport axon terminal The black cargo and the gray cargo require ATP hydrolysis for their motion. The gray cargo is attached to dynein. outward transport The black cargo and the gray cargo are moving along microtubules of opposite polarity. The black cargo moving toward the axon terminal contains a domain that specifically interacts with the tail domain of a particular kind of motor.arrow_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_forwardCa2+-ATPases are integral membrane proteins. They are active transport mechanisms that use the energy derived from ATP hydrolysis to pump calcium ions across the membrane. A specific form of Ca2+-ATPase, ERCA, is located on the endoplasmic reticulum membrane. In which direction does ERCA transport calcium ions? a.) ERCA transports calcium ions from the lumen of the endoplasmic reticulum into the cytoplasm. b.) ERCA transports calcium ions from the cytoplasm into the lumen of the endoplasmic reticulum.arrow_forward
- 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_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_forwardGenetic testing of a 29-month-old boy shows a mutation in the Phe residue at position 508 in the cystic fibrosis transmembrane conductance regulator (CFTCR) gene. Cultured skin fibroblasts from the boy contain an abnormal form of CFTCR protein bound to ubiquitin. Which of the following structures is the most likely site of elimination of these abnormal proteins in this patient? A) Endoplasmic reticulum B) Endosome C) Golgi complex D) Lysosome E) Proteasomearrow_forward
- Which of the following proteins is categorized as a multi-pass transmembrane protein (also called the anion exchange protein, because it exchanges chloride and bicarbonate ions in red blood cells)? band 3.0 protein (in the red blood cell membrane) COX-1 (in the lumenal leaflet of the smooth endoplasmic reticulum) glycophorin A (in the red blood cell membrane) the Ras protein (lipid-linked to the inner plasma membrane) cytochrome c (in the mitochondrion)arrow_forwardMany diseases are characterized by fibrosis, which is excess scarring. This scarring is often caused by too much collagen accumulating in the extracellular matrix. Which of the following strategies is MOST likely to work for preventing fibrosis? O Altering the endomembrane system to increase collagen secretion. O Altering the endomembrane system to decrease detection of the internal start transfer sequence of collagen. O Altering the endomembrane system to increase collagen endocytosis. Altering the nuclear export of collagen via lamins, followed by kinesin-mediated exocytosis.arrow_forwardCadherins are calcium-dependent adhesion proteins. They are homophilic proteins found in cell-cell adhesion. Answer the following. a. Explain what is meant by the term homophilic in this context. b. In what kind of cell-cell junction are cadherins found?arrow_forward
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