The following statements are made regarding apoptosis in the nematode, C. elegans:

A. The human ortholog of C. elegans, CED-9, is overexpressed in a B-cell lymphoma.
B. A ced-9 (gain-of-function); ced-3 (loss-of-function) double mutant will have more than 947 non-gonadal cells.
C. If purified EGL-1 is added to a CED-9/CED-4 complex in vitro, the autoclave of CED-3 does not occur.
D. CED-8 is a multi-spanning plasma membrane protein that is required for externalization of phosphatidylserine.

Which one of the following options represents all correct statements?

Correct option is C

Explanation:

• A is correct: Human Bcl-2, the ortholog of C. elegans CED-9, is known to be overexpressed in B-cell lymphomas, inhibiting apoptosis.

• B is correct: A ced-9 gain-of-function mutation blocks apoptosis leading to excessive cells, and ced-3 loss-of-function prevents cell death execution. Double mutants thus have more than 947 non-gonadal cells.

• C is incorrect: EGL-1 promotes apoptosis by binding CED-9 and releasing CED-4, allowing CED-3 activation. Adding EGL-1 disrupts CED-9/CED-4 complex and triggers CED-3 cleavage in vitro.

• D is correct: CED-8 is a plasma membrane protein required for phosphatidylserine externalization, a key apoptosis marker signaling phagocytosis.

Information Booster:

• C. elegans apoptotic pathway was the first genetically dissected programmed cell death pathway.

• CED-9 (anti-apoptotic) inhibits CED-4 (apoptotic activator), regulating CED-3 caspase activation.

• EGL-1 initiates apoptosis by disrupting CED-9/CED-4.

• Phosphatidylserine exposure on dying cells is mediated by CED-8, marking cells for clearance.

Additional Information on Incorrect Options:

• Statement C incorrectly describes EGL-1’s effect; it promotes CED-3 activation by disrupting CED-9/CED-4.