EBK BIOLOGY
5th Edition
ISBN: 9780133954425
Author: Maier
Publisher: YUZU
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Chapter 6, Problem 2CTS
Summary Introduction
To analyze:
The person should be tested for the cell cycle mutations or not.
Knowing the presence of mutation of proto-oncogenes can be beneficial or not.
Introduction:
The proto-oncogenes are the genes, which regulate the cell cycles and the cell deaths. The main function of the proto-oncogenes is to maintain a specific number of cells. Some of the proto-oncogene regulates the cell cycle by the providing the signals to promote the cell division and some of the proto-oncogenes are involved in the programmed cell death of unwanted or damaged cell.
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Which of the following is an example of a proto-oncogene?
1) cell cycle inhibitor
2) tumor suppressor
3) oncogene
4) repair enzyme
5) growth factor receptor
Put a checkmark next to any of the following scenarios that would make it MORE likely that a cell would divide when it is not supposed to, increasing the chance that it would become cancerous. CHOOSE ALL THAT APPLY.
A) A tumor suppressor gene is over-expressed
B) A cyclin gene is mutated so that it is expressed at all times during the cell cycle
C) A cyclin-dependent kinase gene is mutated so that in the Cdk is no longer dependent on its cyclin
D) A Cdk gene is mutated so that the Cdk protein is not made
E) Mutation of an oncogene that causes it to no longer be expressed
F) A proto-oncogene gene is expressed at higher than normal levels
G) The p53 gene is mutated so that no p53 protein is made
Imagine that there are mutations in the CDK genes such that their gene products are nonfunctional. What effect would this
mutation have on an immature unspecialized blood cell precursor found in the bone marrow?
The cell would not be able to reproduce itself.
The cell would complete the cell cycle using cyclins in the absence of CDKS.
The cell would be able to replicate its DNA but not translate DNA into RNA.
The cell would be able to enter mitosis but not complete it.
The cell would still phosphorylate the CDK-associated target proteins, and would do so more quickly.
Chapter 6 Solutions
EBK BIOLOGY
Ch. 6 - Prob. 1LTBCh. 6 - Prob. 2LTBCh. 6 - A cell that begins mitosis with 46 chromosomes...Ch. 6 - The centromere is a region at which ___________....Ch. 6 - Prob. 5LTBCh. 6 - At metaphase of mitosis, ___________. the...Ch. 6 - Sister chromatids ___________. are two different...Ch. 6 - DNA polymerase ___________. attaches sister...Ch. 6 - Prob. 9LTBCh. 6 - Prob. 10LTB
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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
- Ras is a proto-oncogene that is within the EGF pathway. The EGF receptor can activate the cell division pathway only when the EGF ligand binds to the receptor. A gain of function mutation occurs in only one copy of the Ras gene. What are all the possible consequences of this? Select all that apply. Group of answer choices The cell will undergo constant cell division The cell will still be normal as only one copy of Ras is mutated. Both copies must be mutated for the cell to undergo constant cell division There will be an increase of EGF ligands present in the cell The EGF receptor will always be active even with no EGF ligands bound and activate the pathway Ras will always be active and activate the proteins downstream that will turn on cell division Ras will be under the influence of the EGF receptor and will only activate if the EGF ligand is bound to the receptorarrow_forwardPlease answer question 8arrow_forwardThe protein p53 is activated when the cell's DNA is damaged. p53 helps to arrest the cell cycle in G1, allowing time for the cell to repair its DNA before replicating. p53 does this job by stimulating the synthesis of a protein that inhibits the cyclin-dependent kinase. Mutations that inactivate p53 contribute to 50% of human cancers. Would you classify p53 as a tumor-suppressor gene or a proto-oncogene?arrow_forward
- Cell division cycle mutations render the mutants unable to continue the cell cycle. This phenotype creates a paradox where mutant cells must also be grown in the lab to further identify the gene and study the role of the protein. How do you think this problem can be solved?arrow_forwardWhy would the failure of the p53 tumor supressor gene be more likely to cause cancer in a seventy year old person compared to a ten year old person? Group of answer choices A) The seventy year old is more likely to have pre-existing failures in cell cycle control B) cells divide more rapidly as people get older C) there are fewer mutations in genes controlling the cell cycle in older people D)the p53 gene never works well in old peoplearrow_forwardA protein called p53 is another protein involved in controlling cell division. The protein p53 makes sure that if cells aren't functioning correctly, they don't divide anymore. Some people have damage to their p53 DNA and the protein isn't made correctly anymore. What might be a consequence if a person couldn't make the protein p53? A - Their cells would no longer use oxygen to make energy B - Their cells would no longer divide C - Their cells would make too much carbon dioxide D - Their cells could divide out of controlarrow_forward
- Your friend sends you two cancerous cell lines to examine and determine possible mutations. The results are shown below: Cell Line Mutation WT none (wild type DNA) 1 a deletion at the same region on both copies of chromosome 4 a point mutation in a gene on only one copy of chromosome 7 Based on this data, what type of geńe is mutated in each of the cell lines? Select all that apply O Cell line 2 has a mutation in an oncogene Cell line 1 has a mutation in a tumor suppressor gene Cell line 1 has a mutation in an proto-oncogene Cell line 2 has a mutation in a tumor suppressor genearrow_forward1arrow_forwardI am confused about how stem cell transplants works. If you put a semi differentiated tadpole nucleus in a denucleated egg cell, it’ll develop into a fully formed tadpole, but if you put a fully differentiated tadpole nucleus, it won’t (because the genes have already been expressed in a way where the cytoplasmic determinants cannot operate to the fullest). Then how come in stem cell transplants, you use adult nucleuses that are already developed and transplant them into the denucleated egg cells?arrow_forward
- What is the significance of the cell cycle control system and checkpoints? Explain step by step in your own words. [please make it simple]arrow_forwardA cell inherits a mutation in a gene that results in a transcription factor, called NF-kB, constantly being in its active conformation. When active, NF-kB stimulates the expression of cyclins that promote progression of the cell cycle, regardless of other conditions. As a result of this mutation, how would this cell's phenotype be affected by this mutation? A) This cell would have a cancer phenotype B) This cell would grow larger in size, but would never divide C) This cell would likely undergo apoptosis D) This cell would not duplicate its chromosomes .arrow_forwardYou have two patients with pancreatic cancer. Patient 1 has a KRAS oncogenic mutation; a myc oncogenic mutation and has normal levels of P53. Patient 2 has normal KRAS expression: a myc oncogenic mutation and a tumor suppressor mutation in P53. You have the following therapeutics available Flavopiradol (a CDK inhibitor); CBP-93872 (a G2/M checkpoint inhibitor); Rigosertib; Oncorine; Nutlin a. Which patient would CBP-93872 be the most effective? Explain your answer. b. Which therapeutic(s) would not be expected to be effective in patient 2? For each, explain your answerarrow_forward
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