Question

Of the following mutations, which are likely to cause cell-cycle arrest?

-a mutation in a gene encoding a cell-surface mitogen receptor that makes the receptor active even in the absence of the mitogen
-a mutation that allowed G1-Cdk to be active independently of its phosphorylation status
-a mutation that removed the phosphorylation sites on the Rb protein
-a mutation that inhibited the activity of Rb

Answer 1

The question's mutations likely lead to uncontrolled cell division rather than cell-cycle arrest. Dysfunctional proteins such as mutated mitogen receptors, G1-Cdk, or Rb can fail to properly regulate the cell cycle, causing cells to proceed through the cycle uncontrollably, increasing the risk of cancerous growth.

Step-by-step explanation:

The mutations described in the question are related to cell-cycle regulation and could lead to a cell proceeding uncontrollably through the cell cycle, not cell-cycle arrest. For instance, if a cell surface mitogen receptor is mutated to be permanently active, this can lead to the continuous division of a cell by mimicking the signal that tells a cell to divide when it normally shouldn't. Furthermore, mutations that allow G1-Cdk to be independent of its phosphorylation status or remove the phosphorylation sites on the Rb protein, or inhibit the activity of Rb, weaken the cell's cycle checkpoint controls, leading to unregulated progression through the cell cycle, and potentially cancerous growth.

Damage to proteins like p53, which activates p21 to halt the cell cycle in response to DNA damage, contributes to cell cycle progression despite errors. Without properly functioning checkpoints, such as a fully functional p53, the G1 checkpoint fails to halt the cell, leading to the risk of propagation of mutated genes and accumulation of more mutations, ultimately contributing to tumor growth. Therefore, mutations that alter the activity of these key regulatory proteins disrupt the balanced control mechanisms that ensure healthy cell division.