Correct option is B
The question revolves around the insulin signaling pathway, specifically the PI3K-AKT-FOXO pathway, which is crucial in regulating lifespan and metabolism.
Insulin signaling activates the PI3K pathway, leading to activation of AKT, which in turn inactivates FOXO (a transcription factor involved in longevity and stress resistance).
PTEN negatively regulates the PI3K-AKT pathway by dephosphorylating PIP3, thereby preventing AKT activation.
Mutations in this pathway affect lifespan, as shown in studies on C. elegans and Drosophila.
Analysis of the Statements:
A. A gain of function mutation in AKT makes the organism long-lived. (Incorrect)
AKT activation inhibits FOXO, which reduces stress resistance and longevity.
A gain of function mutation in AKT would increase insulin signaling, further suppressing FOXO, which shortens lifespan instead of increasing it.
B. A FOXO deletion mutation suppresses the long life span of the organism with a reduction of function mutation in the insulin receptor. (Correct)
A reduction-of-function mutation in the insulin receptor extends lifespan because it reduces AKT activation, leading to FOXO activation, which promotes longevity.
However, if FOXO itself is deleted, then the longevity benefit from reduced insulin signaling is lost, confirming this statement as correct.
C. A PTEN deletion mutation suppresses the long life span of the organism with a reduction of function mutation in the insulin receptor. (Correct)
PTEN normally inhibits the PI3K-AKT pathway, which means its deletion increases AKT activity.
If AKT is overactive, it will suppress FOXO, leading to reduced lifespan.
Thus, a PTEN deletion counteracts the lifespan extension caused by reduced insulin signaling, making this statement correct.
D. A loss of function mutation in the FOXO ortholog makes the worms long-lived. (Incorrect)
FOXO activation is required for lifespan extension.
A loss-of-function mutation in FOXO would prevent longevity, not extend it.
Hence, this statement is incorrect.
