Question

If a cell developed a mutation in its MAP2K1 gene (encodes the MEK protein) that prevented MEK from being recognized by phosphatases, how would the EGFR signaling cascade and the cell’s behavior change?

a) Increased phosphorylation of EGFR
b) Decreased activation of Ras
c) Sustained activation of ERK
d) Inhibition of EGFR signaling

Answer 1

A mutation in the MAP2K1 gene can result in sustained activation of MEK and the downstream ERK due to lack of dephosphorylation, leading to uncontrolled cell proliferation and an increased risk of oncogenesis.

Step-by-step explanation:

In the context of the Epidermal Growth Factor Receptor (EGFR) signaling cascade, the MAP2K1 gene encodes for the MEK protein, which is a part of the mitogen-activated protein (MAP) kinase cascade important for cell division, cellular metabolism, and protein expression. A mutation in the MAP2K1 gene that prevents MEK from being recognized by phosphatases would lead to a sustained activation of MEK because it could not be dephosphorylated. This, in turn, would result in sustained activation of the downstream protein ERK, a MAP kinase, because MEK phosphorylates ERK. The ultimate result would be unregulated phosphorylation cascade, which could perpetuate signals for cell proliferation and differentiation without the normal regulatory mechanisms to halt the cascade.

Typically, the phosphorylation cascade is tightly regulated, and dephosphorylation is needed to prevent continuous activation. As such, the mutation described in the MAP2K1 gene leading to a faulty MEK protein would likely result in uncontrolled cell proliferation and potentially oncogenesis if corrective mechanisms fail to intervene.