What would be the phenotype of a cak (Cdk activating kinase) mutant?

In the context of cell cycle regulation, the role of Cdk activating kinase (CAK) is critical for the activation of cyclin-dependent kinases (Cdks). These kinases are essential for the progression through various stages of the cell cycle. CAK phosphorylates Cdks on a specific threonine residue, which is necessary for Cdk activation and subsequent cell cycle progression.

If a mutant lacks functional CAK, the activation of Cdks would be severely impaired. In this scenario, there would be no signal to promote cell cycle progression, leading to an accumulation of cells in specific phases, particularly G2/M, where they would be unable to proceed to mitosis effectively. This lack of progression can lead to phenotypes associated with cell cycle arrest.

The specific phenotype represented by the second option, cdc25-, is pertinent because Cdc25 is a phosphatase that removes inhibitory phosphate groups from Cdks, thus promoting their activation. In a situation where the Cdk activity is influenced by CAK and the resultant mutant lacks this necessary activation, the overall effect would mirror that of a Cdc25 mutant where Cdks remain inactive, resulting in similar cell cycle arrest. Therefore, the phenotype of a cak mutant aligns with that of a