Correct option is C
Explanation:
- Latrunculin is the most suitable choice because it directly inhibits actin polymerization by binding to actin monomers (G-actin) and preventing their incorporation into filaments (F-actin).
- Since PAR protein localization in C. elegans depends on cortical actin dynamics, disrupting actin polymerization with Latrunculin helps study its role in cell polarity.
Information Booster:
- Actin cytoskeleton regulates cell polarity in various organisms, including C. elegans.
- PAR proteins (Partitioning-defective proteins) establish asymmetric cell division in the embryo.
- Latrunculin binds to G-actin and prevents F-actin formation, disrupting actin-based processes.
- Microtubule inhibitors (Taxol, Colchicine) do not target actin and would be ineffective.
- RhoA signaling regulates actin polymerization, affecting cortical contractility and polarity.
Additional Knowledge :
(1) Taxol (Incorrect - Targets Microtubules)
- Taxol stabilizes microtubules by preventing depolymerization.
- Used in cancer therapy to block cell division.
- Does not affect actin polymerization, so it is not suitable for this experiment.
(2) Colchicine (Incorrect - Targets Microtubules)
- Colchicine inhibits microtubule polymerization by binding to tubulin.
- Used to treat gout and inflammation by disrupting microtubule-dependent processes.
- Does not target actin, making it unsuitable for this study.
(3) Latrunculin (Correct - Inhibits Actin Polymerization)
- Directly binds monomeric G-actin, preventing filament formation.
- Commonly used to study actin-dependent processes, including cell polarity, migration, and division.
- Best choice for inhibiting actin polymerization in this experiment.
(4) LY294002 (Incorrect - PI3K Inhibitor)
- LY294002 is a phosphoinositide 3-kinase (PI3K) inhibitor, affecting signaling pathways.
- Used to study cell growth, survival, and metabolism, not cytoskeletal dynamics.
- Not related to actin polymerization, making it an incorrect choice.


