Log out Go to App
Go to App

Learning Materials

Features

Discover

Chapter 16: Problem 10

A genetic variant of the retinoblastoma protein, called PSM-RB (phosphorylation site mutated \(\mathrm{RB}\) ), is not able to be phosphorylated by the action of CDK4/cyclin D1 complex. Explain why PSM-RB is said to have a constitutive growth-suppressing action on the cell cycle.

Short Answer

Expert verified
Answer: PSM-RB (phosphorylation site mutated RB) exhibits a constitutive growth-suppressing action on the cell cycle because it cannot be phosphorylated by the CDK4/cyclin D1 complex due to mutations in its phosphorylation sites. As a result, PSM-RB remains unphosphorylated and in its active form throughout the cell cycle, continuously binding to E2F transcription factors and preventing the transcription of genes required for progression from the G1 phase to the S phase. This perpetual suppression of cell cycle progression by PSM-RB is what gives it its constitutive growth-suppressing action.

Step by step solution

01

Understand the retinoblastoma protein's role in the cell cycle

The retinoblastoma protein (RB) plays a crucial role in regulating the cell cycle by controlling the progression from the G1 phase to the S phase. During the G1 phase, RB binds to E2F transcription factors, effectively inhibiting them. E2F proteins are required for the expression of genes that drive the cell to progress into the S phase. When RB is bound to E2F proteins, it prevents these genes from being transcribed, thereby inhibiting the cell cycle progression.
02

Investigate the significance of RB phosphorylation in the cell cycle

Phosphorylation of RB by cyclin-dependent kinases (CDKs) partnered with cyclins, especially CDK4/cyclin D1 complex, leads to its inactivation. When RB is phosphorylated, it can no longer bind E2F proteins, and these transcription factors are free to activate the expression of genes that drive the cell into the S phase. Therefore, the phosphorylation of RB is necessary for the progression of the cell cycle.
03

Explain the unique feature of PSM-RB

The genetic variant PSM-RB (phosphorylation site mutated RB) is unable to be phosphorylated by the CDK4/cyclin D1 complex. This inability is due to mutations in the phosphorylation sites of RB, which are the target sites for CDK4/cyclin D1. As a result, PSM-RB remains unphosphorylated throughout the cell cycle.
04

Describe the constitutive growth-suppressing action of PSM-RB

Since the genetic variant PSM-RB cannot be phosphorylated by the CDK4/cyclin D1 complex, it remains in its active form throughout the cell cycle. Consequently, it continually binds to E2F transcription factors, preventing the transcription of genes necessary for the progression from the G1 phase to the S phase. This perpetual suppression of cell cycle progression by PSM-RB is referred to as having a constitutive growth-suppressing action on the cell cycle.

Unlock Step-by-Step Solutions & Ace Your Exams!

  • Full Textbook Solutions

    Get detailed explanations and key concepts

  • Unlimited Al creation

    Al flashcards, explanations, exams and more...

  • Ads-free access

    To over 500 millions flashcards

  • Money-back guarantee

    We refund you if you fail your exam.

Start your free trial

Over 30 million students worldwide already upgrade their learning with Vaia!

One App. One Place for Learning.

All the tools & learning materials you need for study success - in one app.

Get started for free

Most popular questions from this chapter

While all cancer cells are proliferative, only some become malignant. Explain this statement.

As part of a cancer research project, you have discovered a gene that is mutated in many metastatic tumors. After determining the DNA sequence of this gene, you compare the sequence with those of other genes in the human genome sequence database. Your gene appears to code for an amino acid sequence that resembles sequences found in some serine proteases. Conjecture how your new gene might contribute to the development of highly invasive cancers.

In this chapter, we focused on cancer as a genetic disease. In particular, we discussed the relationship between cancer, the cell cycle, and mutations in proto-oncogenes and tumor-suppressor genes. Based on your knowledge of these topics, answer several fundamental questions: (a) How do we know that malignant tumors arise from a single cell that contains mutations? (b) How do we know that cancer development requires more than one mutation? (c) How do we know that cancer cells contain defects in DNA repair?

Those who inherit a mutant allele of the \(R B 1\) gene are at risk for developing a bone cancer called osteosarcoma. You suspect that in these cases, osteosarcoma requires a mutation in the second \(R B 1\) allele, and you have cultured some osteosarcoma cells and obtained a cDNA clone of a normal human \(R B 1\) gene. A colleague sends you a research paper revealing that a strain of cancer-prone mice develops malignant tumors when injected with osteosarcoma cells, and you obtain these mice. Using these three resources, what experiments would you perform to determine (a) whether osteosarcoma cells carry two \(R B 1\) mutations, (b) whether osteosarcoma cells produce any pRB protein, and (c) if the addition of a normal \(R B 1\) gene will change the cancercausing potential of osteosarcoma cells?

What are the most significant environmental agents that contribute to human cancers?
See all solutions

Recommended explanations on Biology Textbooks

Heredity

Read Explanation

Ecological Levels

Read Explanation

Organ Systems

Read Explanation

Cell Communication

Read Explanation

Genetic Information

Read Explanation

Substance Exchange

Read Explanation
View all explanations

What do you think about this solution?

We value your feedback to improve our textbook solutions.

Study anywhere. Anytime. Across all devices.

Sign-up for free