In: Biology
Question 37
A cleavage furrow is ________.
a ring of vesicles forming a cell plate |
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the separation of divided prokaryotes |
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a groove in the plasma membrane between daughter nuclei |
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the space that is created between two chromatids during anaphase |
Question 38
What does p53 do?
stops the cell cycle at metaphase when the cells DNA is damages |
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stops the cell cycle at G2 when the cell’s DNA is damages |
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initiates cytokinesis |
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none of the above are correct |
Question 39
_________________ inhibits the cell cycle and promotes apoptosis.
proto-oncogenes |
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oncogenes |
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tumor suppressor genes |
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telomeres |
Question 40
______________ tumors are:
encapsulated |
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do not invade neighboring tissue or spread |
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undergo metastasis |
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none of the above |
Question 37)
A cleavage furrow is the space that is created between two chromatids during anaphase .
Cytokinesis begins in anaphase and ends in telophase reaching completion as the next interphase begins. The first visible change of cytokinesis in an animal cell is the sudden appearance of a cleavage furrow on the cell surface.Animal cell cleavage furrow formation is caused by a ring of actin microfilaments called the contractile ring, which forms during early anaphase. The bridge is then broken and resealed to form two identical daughter cells during cytokinesis.
Question 38:
stops the cell cycle at G2 when the cell’s DNA is damages.
Damage to DNA and other external factors are evaluated at the G1 checkpoint, if conditions are inadequate the cell will not be allowed to continue to the S phase of interphase. The G2 checkpoint ensures all of the chromosomes have been replicated and that the replicated DNA is not damaged before cell enters mitosis.
Cells in which p53 is deleted or mutated lose the G1 checkpoint and no longer arrest at the G1/S transition. Although they maintain a G2 arrest, this arrest can decay over time thus allowing cells to enter mitosis with unrepaired DNA damage and mutations that increase the risk of progression to malignancy.
Long-term maintenance of the G2 arrest is also mediated by p53, which is stabilized in response to DNA damage. CDK1 is directly inhibited by three transcriptional targets of p53: p21, Gadd45, and 14-3-3σ.
Question 39:
tumor suppressor genes inhibits the cell cycle and promotes apoptosis.
The tumor-suppressor protein p53 accumulates when DNA is damaged due to a chain of biochemical factors. Part of this pathway includes alpha-interferon and beta-interferon, which induce transcription of the p53 gene, resulting in the increase of p53 protein level and enhancement of cancer cell-apoptosis.
Question 40:
Encapsulated.
Benign neoplasms typically have smooth borders, are sharply demarcated from the normal tissue at the tumor site, and are frequently encapsulated by a fibrous capsule that forms a barrier between the neoplastic cells and the host tissue.