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The p53 protein can activate genes involved in apoptosis. Review Concept 11.5, and discuss how mutations in genes coding for proteins that function in apoptosis could contribute to cancer.

Short Answer

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The p53 tumor suppressor genes activate apoptosis. However, a mutation in the p53 genes can suppress the mechanism of apoptosis that leads to a rapid division of cells resulting in cancer.

Step by step solution

01

Description of p53 protein

p53 is the gene that controls cell division and growth. The proteins produced from p53 genes are those involved in the control of the cell cycle mechanisms.

02

Apoptosis

Every cell tends to divide to maintain the population of new cells. However, cell multiplication has to stop at a certain point, and the cells have to enter the death phase.

The process of cell death is regulated by certain internal body mechanisms called apoptosis, which is otherwise called programmed cell death.

03

Removal of cells by apoptosis

Cells are exposed to damage frequently, which needs to be removed from the regular cell cycle. These cells enter the apoptotic pathway and get eliminated from the body.

p53 is a gene that activates apoptosis by the transcriptional activation mechanism of the apoptotic protein. It acts as a checkpoint mechanism to eliminate the damaged cells.

04

Mutation in the P53 gene related to cancer

Mutation in the p53 gene that involves apoptosis can result in the suppression of apoptotic control. The loss in apoptotic control may lead to the rapid multiplication of cells without cell death, which causes the accumulation of cells forming a tumor mass.

It also leads to the growth of damaged or unrepaired cells that result in defective metabolic activities. Thus, a mutation in the p53 gene may block the apoptotic pathway. This may not remove the damaged cell from the cell cycle and eventuallyresult in tumor formation.

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Most popular questions from this chapter

The diagram below five genes, including their enhancers, from the genome of a certain species. Imagine that pink, blue, green, black, grey and dark blue activator proteins exist that can bind to the approximately colour-coded control elements in the enhancers of these genes.

(a) Draw an X above enhancer elements (of all the genes) that would have activators bound in a cell where only gene five is transcribed. Identify which coloured activators would be present.

(b) Draw a dot above all enhancer elements that would have activators bound in a cell where the green, blue, and yellow activators are present. Identify which gene(s) would be transcribed.

(c) Imagine that genes 1, 2, and 4 codes for nerve-specific proteins, and genes 3 and 5 are skin-specific. Identify which activators would have to be present in each cell type to ensure transcription of the appropriate genes.

Prostrate cells usually require testosterone and other androgens to survive. But some prostate cancer cells thrive despite treatments that eliminate androgens. One hypothesis is that estrogen, often considered a female hormone, may be activating genes normally controlled by androgen in these cancer cells. Describe one or more experiments to test this hypothesis. (See Figure 11.9 to review the action of these steroid hormones).

Compare miRNAs and siRNAs, including their functions.

Cell differentiation always involves

(A) transcription of the myoD gene.

(B) the movement of cells.

(C) the production of tissue-specific factors

(D) the selection loss of certain genes from the genome.

Suppose the mRNA being degraded in Figure 18.14 coded for a protein that promotes cell division in a multi-cellular organism. What would happen if a mutation disabled the gene for the miRNA that triggers this degradation?

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