EBK BROCK BIOLOGY OF MICROORGANISMS
15th Edition
ISBN: 8220103633352
Author: Stahl
Publisher: PEARSON
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Chapter 27.6, Problem 1MQ
Define polymorphism and polygeny as they apply to MHC genes.
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Variable addition and subtraction of nucleotides at the junctions between gene segments contributes to the diversity of [Qi] the third hypervariable region. The addition and subtraction of nucleotides at the junctions between V, D, and J gene segments creates antibody proteins with wide variations in the numbers of amino acids in their CDR3 regions. This variability in CDR3 length is important as:
Overall variability in CDR3 sequence is needed to create a sufficiently diverse antibody repertoire.
The CDR3 region is more important in binding antigen than the CDR1 and CDR2 regions are.
Some light chains bind better to heavy chains with longer CDR3 region sequences.
Longer CDR3 sequences generally create antibodies with higher affinity for the antigen.
Some antibodies bind relatively flat surfaces and others bind deep clefts in the antigen.
The immunoglobulin molecules of a particular mammalian species have kappa and lambda light chains and heavy chains. The kappa gene consists of 250 V and 8 J segments. The lambda gene contains 200 V and 4 J segments. The gene for the heavy chain consists of 300 V, 8 J, and 4 D segments. If just somatic recombination and random combinations of light and heavy chains are taken into consideration, how many different types of antibodies can be produced by this species?
Severe combined immunodeficiency disease is a life-threatening genetic disease in which children are born with defective B-cell and Tcell function. These children are susceptible to severe infections, such as pneumonia, meningitis, or blood-borne infections. They can also be infected and sickened by live viruses that are present in some vaccines. Children with some forms of severe combined immunodeficiency disease have mutations in their RAG1 or RAG2 genes. Provide a possible explanation for how mutations in these genes might lead to the symptoms of this disorder
Chapter 27 Solutions
EBK BROCK BIOLOGY OF MICROORGANISMS
Ch. 27.1 - Prob. 1MQCh. 27.1 - Prob. 2MQCh. 27.1 - Distinguish between clonal deletion and clonal...Ch. 27.1 - QWhy is it necessary that all three defining...Ch. 27.2 - Identify the intrinsic and extrinsic properties of...Ch. 27.2 - Describe an epitope recognized by an antibody, and...Ch. 27.2 - Give an example for each: natural and artificial...Ch. 27.2 - QWhat properties are required for a vaccine to...Ch. 27.3 - Summarize antibody production starting with...Ch. 27.3 - Differentiate among antibody classes using...
Ch. 27.3 - Prob. 3MQCh. 27.3 - QDescribe the structural and functional...Ch. 27.4 - Draw a complete Ig molecule and identify...Ch. 27.4 - Describe antigen binding to the CDR1, 2, and 3...Ch. 27.4 - Describe the recombination events that produce a...Ch. 27.4 - QWhich Ig chains are used to construct a complete...Ch. 27.5 - Identify the cells that display MHC class I and...Ch. 27.5 - Compare the MHC I and MHC II protein structures...Ch. 27.5 - Define the sequence of events for processing and...Ch. 27.5 - QDescribe the basic structure of class I and class...Ch. 27.6 - Define polymorphism and polygeny as they apply to...Ch. 27.6 - How does a single MHC protein present many...Ch. 27.6 - QPolymorphism implies that each different MHC...Ch. 27.7 - Prob. 1MQCh. 27.7 - Identify diversity-generating mechanisms unique to...Ch. 27.7 - Describe and compare the structural features of Ig...Ch. 27.7 - QWhat diversity-generating mechanisms function to...Ch. 27.8 - Describe the mechanism used by Tc cells to...Ch. 27.8 - Describe the effector system (the cell-killing...Ch. 27.8 - Compare and contrast the roles and activities of...Ch. 27.8 - QWhat mechanism do Tc cells use to identify and...Ch. 27.9 - Discriminate between immediate hypersensitivity...Ch. 27.9 - Provide examples and mechanisms for an...Ch. 27.9 - QHow do immediate and delayed-type...Ch. 27.10 - Describe the binding site for superantigens on T...Ch. 27.10 - Compare and contrast the immunodeficiency observed...Ch. 27.10 - Prob. 3MQCh. 27.10 - Prob. 1CRCh. 27 - Antibodies of the IgA class are probably more...Ch. 27 - Prob. 2AQCh. 27 - Polymorphism implies that each different MHC...Ch. 27 - What problems would arise if a person had a...
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- Hyper-IgE syndrome, also known as Job’s syndrome, is an immunodeficiency disease resulting from the lack of function of a single gene (gene ‘X’). Patients with this disease are highly susceptible to infections with extracellular bacteria and fungi, most frequently including Staphylococcus aureus infections and Candida albicans infections in the skin. Analysis of the various immune cell compartments indicates that these patients have normal numbers of each cell lineage (i.e., CD4 and CD8 T cells, B cells, monocytes, dendritic cells, NK cells, granulocytes, etc.), and normal levels of IgG, IgA, and IgM antibodies, but higher than normal levels of IgE. Given this information, name a likely component of the immune response that could be impaired in these patients.arrow_forwardMany antibodies exhibit dosage, discuss the antibodies that exhibit dosage and how it is demonstrated in heterozygous/homozygous cells. Additionally, in some cases, if an antibody is just starting to develop, it may not react with a heterozygous cell, discuss the reasons for this.arrow_forwardFlow cytometry analysis was performed on the blood of an individual known to have been recently exposed to both rhinovirus (RV) and Mycobacterium tuberculosis (M.tb; an intracellular bacterial pathogen). Although an effective T cell response against RV was detected, a T cell response against M.tb was absent. Subsequently, genetic testing was performed, and the individual was found to possess two mutations. Below, indicate the MOST LIKELY mutations. A. T-bet; IL-12 B. CD28: IL-2Ra C. RORyT: IL-17 D. CD3: CD4arrow_forward
- Defects in antigen receptor gene rearrangement can result in SCID (severe combined immunodeficiency). Infants with RS-SCID (radiation-sensitive SCID) generally require treatment by bone marrow transplantation from a healthy donor. In this treatment, hematopoietic stem cells from the donor will give rise to normal B and T lymphocytes, thereby restoring normal immune function. However, the bone marrow transplantation treatment does not alter the high incidence of cancer in these patients. Why not?arrow_forwardusing a molecular genetic approach how can one generate a mouse missing an adaptive immune responsearrow_forwardExplain how hematopoietic stem cells were experimentally shown to be both multipotent and capable of self-renewal.arrow_forward
- Which among the mammalian expression system and the bacterial expression system is better in producing recombinant erythropoietin? What is transfection?arrow_forwardThe following interactions occur during the expression and secretion of an antibody heavy-chain protein. Number them in the order that each takes place for the first time. A spliceosome interacts with the 5th intron (but not with the 6th). A B cell-specific protein bound to an enhancer interacts with a protein complex bound to the promoter. A signal recognition particle (SRP) interacts with a signal peptide sequence. A recombinase acts on copies of a specific DNA sequence in the gene.arrow_forwardAtaxia-telangiectasis (ATM) is a rare genetic neurodegenerative disease. About 20% of people with ATM develop acute lymphocytic leukemia or lymphoma, cancers of the immune-system cells. Cells in many of these cancers exhibit chromosome rearrangements, with chromosome breaks occurring at antibody and T-cell-receptor genes (A. L. Bredemeyer et al. 2006. Nature 442:466–470). Many people with ATM also have a weakened immune system, which makes them susceptible to respiratory infections. Research has shown that the locus that causes ATM has a role in the repair of double-strand breaks. Explain why people who have a genetic defect in the repair of doublestrand breaks might have a high incidence of chromosome rearrangements in their immune-system cells and why their immune systems might be weakened.arrow_forward
- You have been asked to engineer a protein (which is not animmunoglobulin) that is capable of binding to a given protein target.Devise a strategy and discuss the main molecular screeningapproaches required.arrow_forwardgamma:delta T-cell receptors are also generated by gene rearrangement. Some T cells express gamma:delta T-cell receptors rather than alpha:beta T-cell receptors. The organization of the a locus and the d locus helps to ensure that each T cell cannot express both types of T-cell receptors. The mechanism involved is that: The rearrangement of a T-cell receptor a gene deletes the d locus on that allele. The rearrangement of a T-cell receptor d gene deletes the a locus on that allele. The RAG recombinase enzymes are down-regulated immediately after the first T-cell receptor genes rearrange. The a:b T-cell receptor signals the T cell to delete the d locus. The g:d T-cell receptor signals the T cell to delete the a locus.arrow_forwardIn rare instances, B cells can be found that have two immunoglobulin light chain alleles, both of which are rearranged in frame, and can encode functional light chain proteins. Yet, on the surface of the B cell, only one of the two light chain proteins is detected in the membrane-bound immunoglobulin receptor. The reason these rare cells have two functional light chain rearrangements but only express one of the two light chains as part of the B-cell receptor is: One of the two light chains is formed from rearrangement of a V gene segment that is a pseudogene. One of the two light chain proteins doesn’t form a stable complex with the heavy chain expressed in this cell. One of the two light chain alleles is not transcribed efficiently, and produces only low levels of protein. One of the two light chain alleles uses a V gene segment that is not targeted very often by the RAG recombinase. One of the two light chains is rapidly degraded after synthesis due to improper folding.arrow_forward
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