Genetics: Analysis and Principles
5th Edition
ISBN: 9780073525341
Author: Robert J. Brooker Professor Dr.
Publisher: McGraw-Hill Education
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Chapter 25, Problem 21CONQ
Summary Introduction
To review:
The expected cell lineage, if the heterochronic type of mutation has the followingeffects.
Too early turning of one cell division by gene X.
Too late turning of one cell division by gene X.
Introduction:
Mutations are the sudden changes that occur in the sequences of
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Although slow acting retroviruses lack oncogenes, retroviral infection can activate proto oncogenes leading to oncogenesis.
a. Describe the mechanism of proto-oncogenes activation that can result from with infection with slow acting retroviruses.
b. In what other ways can proto-oncogenes be converted to oncogenes?
SCENARIO:
MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side.
She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer.
Past Medical History
Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up.
Past Surgical History:
Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago.
Medications:
Glyburide, 5mg PO BID
Verapamil SR, 240mg PO daily
Furosemide, 40mg PO daily
Allergies: NKDA
Physical Examination:
GEN: Well-developed, obese…
SCENARIO:
MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side.
She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer.
Past Medical History
Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up.
Past Surgical History:
Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago.
Medications:
Glyburide, 5mg PO BID
Verapamil SR, 240mg PO daily
Furosemide, 40mg PO daily
Allergies: NKDA
Physical Examination:
GEN: Well-developed, obese…
Chapter 25 Solutions
Genetics: Analysis and Principles
Ch. 25.1 - Prob. 1COMQCh. 25.1 - Prob. 2COMQCh. 25.1 - Which of the following is the correct order for...Ch. 25.2 - Prob. 1COMQCh. 25.2 - Prob. 2COMQCh. 25.2 - Prob. 3COMQCh. 25.2 - Prob. 4COMQCh. 25.3 - Prob. 1COMQCh. 25.3 - Prob. 2COMQCh. 25.3 - 3. Myogenic bHLH proteins are ___________ that...
Ch. 25.4 - Prob. 1COMQCh. 25.4 - Prob. 2COMQCh. 25.5 - 1. A key event that initially determines female or...Ch. 25.5 - Prob. 2COMQCh. 25 - 1. What four types of cellular processes must...Ch. 25 - Prob. 2CONQCh. 25 - Prob. 3CONQCh. 25 - 4. Which of the following statement(s) is/are true...Ch. 25 - Discuss the morphological differences between the...Ch. 25 - Prob. 6CONQCh. 25 - Explain what a morphogen is, and describe how it...Ch. 25 - 8. What is positional information? Discuss three...Ch. 25 - Prob. 9CONQCh. 25 - Prob. 10CONQCh. 25 - 11. Describe the function of the Bicoid protein....Ch. 25 - With regard to development, what are the roles of...Ch. 25 - Discuss the role of homeotic genes in development....Ch. 25 - Describe the molecular features of the homeobox...Ch. 25 - What would you predict to be the phenotype of...Ch. 25 - Prob. 16CONQCh. 25 - If a mutation in a homeotic gene produced the...Ch. 25 - 18. Explain how loss-of-function mutations in the...Ch. 25 - What is the difference between a maternal-effect...Ch. 25 - Prob. 20CONQCh. 25 - Prob. 21CONQCh. 25 - Prob. 22CONQCh. 25 - 23. Discuss the similarities and differences...Ch. 25 - 24. What is cell differentiation? Discuss the role...Ch. 25 - Prob. 25CONQCh. 25 - What is a totipotent cell? In each of the...Ch. 25 - 27. What is a meristem? Explain the role of...Ch. 25 - Prob. 28CONQCh. 25 - Predict the phenotypic consequences of each of the...Ch. 25 - 30. Explain how alternative splicing affects sex...Ch. 25 - Prob. 1EQCh. 25 - Compare and contrast the experimental advantages...Ch. 25 - 3. What is meant by the term cell fate? What is a...Ch. 25 - 4. Explain why a cell lineage diagram is necessary...Ch. 25 - Explain the rationale behind the use of the bag of...Ch. 25 - Prob. 6EQCh. 25 - Take a look at question 2 in More Genetic TIPS...Ch. 25 - All of the homeotic genes inDrosophilahave been...Ch. 25 - Prob. 9EQCh. 25 - wo techniques commonly used to study the...Ch. 25 - Prob. 11EQCh. 25 - Prob. 12EQCh. 25 - 13. Another way to study the role of proteins...Ch. 25 - 14. Why have geneticists used reverse genetics to...Ch. 25 - Prob. 1QSDCCh. 25 - Prob. 2QSDCCh. 25 - Prob. 3QSDC
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- SCENARIO: MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side. She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer. Past Medical History Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up. Past Surgical History: Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago. Medications: Glyburide, 5mg PO BID Verapamil SR, 240mg PO daily Furosemide, 40mg PO daily Allergies: NKDA Physical Examination: GEN: Well-developed, obese…arrow_forwardSCENARIO: MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side. She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer. Past Medical History Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up. Past Surgical History: Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago. Medications: Glyburide, 5mg PO BID Verapamil SR, 240mg PO daily Furosemide, 40mg PO daily Allergies: NKDA Physical Examination: GEN: Well-developed, obese…arrow_forwardSCENARIO: MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side. She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer. Past Medical History Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up. Past Surgical History: Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago. Medications: Glyburide, 5mg PO BID Verapamil SR, 240mg PO daily Furosemide, 40mg PO daily Allergies: NKDA Physical Examination: GEN: Well-developed, obese…arrow_forward
- SCENARIO: MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side. She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer. Past Medical History Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up. Past Surgical History: Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago. Medications: Glyburide, 5mg PO BID Verapamil SR, 240mg PO daily Furosemide, 40mg PO daily Allergies: NKDA Physical Examination: GEN: Well-developed, obese…arrow_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will not…arrow_forwardIn a few sentences, describe how p53 guards the genome. Include at least two specific ways that p53 guards the genome. In a few more sentences, describe the structure and function of the p53 protein. Structure: what domains are present in the p53 protein? Do p53 work as a single protein or as part of a complex? Function: what do the different domains do? How can p53 do so many different things?arrow_forward
- In 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_forwardIn tumor cells obtained from patients with Burkittlymphoma, a cancer of the immune system’s B cells,the myc gene often appears close to one of the breakpoints of a reciprocal translocation between chromosomes 8 and 14. In this translocated position, myc is expressed at a higher-than-normal level. Scientists hypothesize that Myc protein overexpression in B cellscontributes to lymphoma formation.a. Explain how transgenic mice produced using pronuclear injection could be used to test this hypothesis. (Assume that you previously cloned a generegulatory region that is active specifically in Bcells throughout the life of the mouse.)b. Suppose you wanted to overexpress Myc only inthe immune cells of mice, starting at one week ofage. To restrict Myc transcription spatially, youwill use same promoter described in part (a). Torestrict Myc transcription temporally, you will usea cre transgene whose expression is controlled byheat shock (hs-cre). Describe the mouse you wouldcreate to accomplish…arrow_forwardSuppose that a particular species of vertebrate animal has immunoglobulin heavy-chain genes that include 55 V segments, 21 D segments, and 8 J segments, and has immunoglobulin light-chain genes that include 41 V segments and 6 J segments. How many different immunoglobulin structures could be produced by mature B-lymphocytes? (Assume that segments are spliced without any junctional variation or imprecision).arrow_forward
- /20. In class, we discussed diffferent types of genetic change that can cause a normal gene (proto- oncogene) to become a cancer-causing gene (oncogene), Which of the following would not be a cause? A) translocation or transposition (movement of DNA within the same genome) B) gene ampliffication (increased number of copies of a given gene) C) epigenetic change D) point mutation that changes the gene's product E) loss of telomeres during DNA replication ancer?arrow_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. eg Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will…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
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