Shown below is an activation pathway for Gene X, needed for entry into S phase o

Question

Shown below is an activation pathway for Gene X, needed for entry into S phase of the cell cycle. Binding of growth factor to the receptor (Protein 1) causes the receptor to phosphorylate Protein 2. Asaresult, Protein 2 releases Protein 3, which is then free to enter the nucleus and activate transcription of Gene X. Gene X turns on genes that allows passage through the G1/s checkpoint and commits the cell to divide. Is a gain-of-function mutation or a loss-of-function mutation in one allele of a gene more likely to promote progression toward cancer? In one sentence explain your answer. Is a mutation in one allele that causes protein 1 to always be stimulated (even when no growth factor is present) enough to progress the cell towards cancer? In one sentence explain what would happen in the pathway (proteins 2 and 3 and transcription of Gene X) as a result of the mutation. Would the mutation of protein 1 described in part b be considered a proto-oncogene or a tumor-suppressor? Would it be considered dominant or recessive? In hereditary forms of cancer (ex. Colon cancer, breast cancer, retinoblastoma), what type of genes (proto-oncogenes or tumor-suppressors) are the mutations in? Why are some members of these families at a higher risk of developing cancer than the general population?

Explanation / Answer

Gain of functional mutation and loss of functional mutation will promote progression towards cancer because of the consequence of dominant mutation which is observed in heterozygous condition carrying one mutant and one normal allele. Dominant mutants are leading to a mutant phenotype which is associated with dominant mutation causes either loss or gain of function. Yes, the mutation in one allele is enough to progress the cell towards cancer. If protein A will be mutated then phosphorylation will not take place and transportation of protein will not occur. The genes will be transcriptionally over expressed. It will become proto-oncogene because of mutations and increased expression.It will consider as a dominant. Tumor suppressor genes. Some members of these families have higher risk because of the epigenetically caused DNA repair deficiency.

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