Which factor most likely causes a cell to be arrested at the G2 phase?

Which factor most likely causes a cell to be arrested at the G2 phase?

• A. The kinetochore microtubules have been unable to capture all chromosomes
• B. The tumor suppressor protein p53 has been activated to promote synthesis of the p21 Cdk inhibitor protein
• C. The APC ubiquitin ligase has added a polyubiquitin tag to the protein securin
• D. The cell has a mutation in Cdc25 phosphatase, where this protein has lost all its functions

Answer: (D)

The reason for the choice emphasizing the mutation in Cdc25 phosphatase as the cause for a cell being arrested at the G2 phase relates to the critical role this protein plays in regulating the cell cycle. Cdc25 is a phosphatase that activates cyclin-dependent kinases (CDKs) by removing inhibitory phosphate groups. Specifically, at the G2/M checkpoint, Cdc25 is responsible for dephosphorylating cyclin B/CDK complexes, which allows the cell to proceed into mitosis. If Cdc25 phosphatase has a mutation that results in a complete loss of function, it would be unable to activate the necessary CDKs, thereby preventing the initiation of mitosis. This inability to transition from the G2 phase into M phase would lead to cell cycle arrest, as the cell cannot properly prepare for division. In contrast, while other factors mentioned can influence cell cycle progression, such as issues with microtubule attachment to kinetochores or the activation of p53 leading to the expression of Cdk inhibitors, they do not directly cause an arrest at the point relating to Cdc25's function in the G2/M transition. The APC ubiquitin ligase and the tagging of securin also

The reason for the choice emphasizing the mutation in Cdc25 phosphatase as the cause for a cell being arrested at the G2 phase relates to the critical role this protein plays in regulating the cell cycle. Cdc25 is a phosphatase that activates cyclin-dependent kinases (CDKs) by removing inhibitory phosphate groups. Specifically, at the G2/M checkpoint, Cdc25 is responsible for dephosphorylating cyclin B/CDK complexes, which allows the cell to proceed into mitosis.

If Cdc25 phosphatase has a mutation that results in a complete loss of function, it would be unable to activate the necessary CDKs, thereby preventing the initiation of mitosis. This inability to transition from the G2 phase into M phase would lead to cell cycle arrest, as the cell cannot properly prepare for division.

In contrast, while other factors mentioned can influence cell cycle progression, such as issues with microtubule attachment to kinetochores or the activation of p53 leading to the expression of Cdk inhibitors, they do not directly cause an arrest at the point relating to Cdc25's function in the G2/M transition. The APC ubiquitin ligase and the tagging of securin also