In other words, the master regulator initiates a program of gene expression that narrow the potential fates of the precursor's cells’ descendants to the type of cells that participate in the organ’s function. Question: Once a master regulator gene is turned on in some cells and not in others, how do cells “remember” that pattern through all the cell division that occur to form a specific organ?

In other words, the master regulator initiates a program of gene expression that narrow the potential fates of the precursor's cells’ descendants to the type of cells that participate in the organ’s function. Question: Once a master regulator gene is turned on in some cells and not in others, how do cells “remember” that pattern through all the cell division that occur to form a specific organ?

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section: Chapter Questions

Problem 15QP: Which of the following mutations will result in cancer? a. homozygous recessive mutation in a...

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Describe how Ras and p53 can alter the simplified genetic pathway controlling cell division shown below. For each of the two genes, would uncontrolled cell division result from a loss-of-function or a gain-of-function mutation? growth factors - receptors - cyclins - cyclin-dependent kinases - cell division
Describe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?
A 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 .
Explain the difference between asymmetric and symmetric cell division. When the pool of stem cells for a particular tissue needs to expand, which of these two cell division mechanisms is utilized?
One important biological effect of a large dose of ionizing radiation (like X-rays) is to halt cell division. How does this occur? To answer this question, state the name and role of 2 specific and important proteins involved in the process. What happens if a cell has a mutation that prevents it from halting cell division after be irradiated? Be specific and detailed. An adult human who has reached maturity will die within a few days of receiving a radiation dose large enough to stop cell division. What does that tell you about cell division? In addition, name 2 different/unique cell types that would be primarily affected.
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Human cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice. State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth. the mitogenic signaling pathway controlled by Ras. the cell cycle checkpoint controlled by pRb. the alarm pathway controlled by p53. the telomere maintenance pathway controlled by hTERT. the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.
Distinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.
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