Final answer:
In yeast Saccharomyces pombe, a loss of function mutation preventing M-Cdk activation results in the cell's inability to enter the M-phase, leading to continuous growth without proper regulation. This cellular behavior typically results from defects in cell cycle checkpoints or regulation mechanisms. Mutations that disrupt the normal cell cycle can contribute to the accumulation of oncogenes and faulty tumor suppressor genes, promoting tumor growth.
Step-by-step explanation:
In the case of the yeast Saccharomyces pombe, a loss of function mutation can lead to a situation where M-CDK (mitotic cyclin-dependent kinase) is not activated, preventing the cell from entering the M-phase of the cell cycle. This introduction of a mutation can stem from a defect in any one of the several control mechanisms, such as the G1 checkpoint being compromised due to a non-functional p53, which normally is responsible for triggering p21 production to block CDK activation. Without this regulation, cells ignore the internal and external signals that would typically prevent them from proceeding to the next phase, leading to uninterrupted cell cycle progression and potentially resulting in the accumulation of oncogenes and non-functional tumor suppressor genes, contributing to tumor growth.
Another example of mutations affecting cell cycle regulation is the one where a mutation results in the production of an abnormal cyclin-dependent kinase at the G2/M checkpoint. This could lead to an array of consequences, including the inability of cells to properly enter and complete mitosis. Finally, it's important to note that yeasts like Saccharomyces pombe, although simpler eukaryotic organisms, have complex cell cycle regulatory mechanisms similar to those in multicellular organisms, despite lacking certain components such as tyrosine kinases.