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A mouse has one normal E2F allele, and one mutant “null” E2F…

A mouse has one normal E2F allele, and one mutant “null” E2F allele (meaning that a totally useless protein is coded for, instead of a normal E2F allele). How will the pathway leading to the activation of the cell cycle by mitogens be impacted in this mouse, and what will the overall effect be on the mouse’s cells, and on the mouse? (Check all that apply) A figure simplified from lecture and a description of how mitogens activate the cell cycle in senescent cells is included below to help. (Note: This is a “reading/lecture comprehension” question, and not a question that tests your memorization skills. It is important to me that students understand the dynamic nature of signaling pathways — how they can be regulated and disrupted. I am not trying to trick you!)     Description of pathway: The default state of cells in our body is to be senescent (not actively engaged in the cell cycle). Mitogens are proteins (ligands) that stimulate senescent cells into entering the cell cycle. How this happens: A mitogen binding to its receptor activates Ras. Ras activates MAP kinase. These leads to increased transcription of several genes including the transcription factor Myc. Myc promotes transcription of Cyclin D. Cyclin D binds G1-Cdk, activating it. Activated G1-Cdk inactivates Rb protein. In its active state, Rb protein binds to and inactivates E2F protein. When Rb protein is inactivated, it releases and allows activation of E2F protein. E2F protein promotes transcription of genes required for S-phase to occur. This results in the translation of cyclins associated with S-phase. These cyclins bind to and activate S-Cdk. Activated S-Cdk promotes DNA synthesis in a variety of ways.