18. In eukaryogtes, cytokinesis is inhibited by (a) Cytochalasin D (b) Vinblastine (c) Nocodazole (d) Colchicines

18. In eukaryogtes, cytokinesis is inhibited by
(a) Cytochalasin D (b) Vinblastine
(c) Nocodazole (d) Colchicines

Here’s a SEO-optimized article on the topic, tailored for educational searches in biotechnology and cell biology. I’ve incorporated the key phrase “cytokinesis is inhibited by” naturally, selected a descriptive title, generated a slug, and included a meta description. The content explains the correct answer with evidence from cell biology mechanisms, while covering all options for comprehensive understanding.


Understanding Cytokinesis in Eukaryotes

Cytokinesis marks the final stage of cell division in eukaryotes, where the cytoplasm divides to form two daughter cells. In animal cells, this process relies on a contractile ring of actin and myosin filaments that pinches the cell membrane inward. Disruptions to this machinery halt cytokinesis, leading to binucleate cells. Multiple choice questions (MCQs) like “In eukaryotes, cytokinesis is inhibited by” test knowledge of drugs targeting cytoskeletal elements.

The Correct Answer: Cytochalasin D

Answer: (a) Cytochalasin D

Cytochalasin D specifically inhibits cytokinesis by binding to the barbed ends of actin filaments, preventing actin polymerization. This disrupts the formation and contraction of the actin-myosin ring essential for cytoplasmic cleavage in eukaryotic cells.

Experiments show that treating mammalian cells (e.g., HeLa cells) with Cytochalasin D during mitosis allows nuclear division (karyokinesis) but blocks cytokinesis, resulting in multinucleated cells. Studies in journals like Journal of Cell Biology confirm its potency at nanomolar concentrations, making it a standard tool in cell biology research for isolating mitosis from cytokinesis.

Why Not the Other Options?

While all options disrupt microtubules, they primarily affect karyokinesis, not cytokinesis directly. Here’s a breakdown:

  • (b) Vinblastine: This alkaloid binds tubulin dimers, depolymerizing microtubules. It arrests cells in metaphase by preventing spindle formation, inhibiting mitosis overall. Cytokinesis proceeds if karyokinesis completes, so vinblastine does not specifically block it.

  • (c) Nocodazole: A synthetic benzimidazole, nocodazole reversibly depolymerizes microtubules, disrupting the mitotic spindle and activating the spindle assembly checkpoint. Like vinblastine, its primary effect is on chromosome segregation, with cytokinesis unaffected once past metaphase.

  • (d) Colchicine: Derived from autumn crocus, colchicine binds tubulin to inhibit microtubule polymerization, causing metaphase arrest. Historical studies (e.g., on sea urchin eggs) show it blocks karyokinesis but allows cytokinesis furrowing in some cases, confirming it’s not a cytokinesis inhibitor.

Drug Target Primary Effect Impact on Cytokinesis
Cytochalasin D Actin filaments Prevents polymerization Inhibited (contractile ring disrupted)
Vinblastine Microtubules Depolymerization Minimal (spindle-focused)
Nocodazole Microtubules Depolymerization Minimal (spindle-focused)
Colchicine Microtubules Polymerization block Minimal (spindle-focused)

Key Takeaways for Biotech Students

Cytochalasin D stands out because cytokinesis in eukaryotes depends more on microfilaments (actin) than microtubules post-mitosis. Microtubule drugs like the others excel in karyokinesis inhibition, a common MCQ distractor. For exams or lab work in microbiology and bioengineering, remember: actin for cleavage, tubulin for spindles.

This distinction aids research in microbial growth kinetics and mammalian cell culture, where precise cell division control is crucial.

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