In Cytokinesis What Happens?

Cytokinesis is a vital stage of the cell cycle that divides the cytoplasm of a parental cell into two distinct daughter cells. It occurs in coordination with the nuclear division phases of mitosis in animal cells and meiosis in germ cells, ensuring that each new cell receives one copy of the divided nucleus. But what exactly happens during cytokinesis and why is it so critical to cell replication?

What Triggers Cytokinesis?

Cytokinesis initiation is closely tied to the progression of nuclear division in mitosis and meiosis. It begins during the late anaphase stage, when chromosomes have separated and migrated to opposite poles of the cell, and continues through telophase as nuclear envelopes reform around each set of chromosomes.

The trigger for cytokinesis depends on the cell type:

• Animal Cells: In animal cells, a contractile ring made of actin and myosin filaments forms beneath the plasma membrane at the former metaphase plate. The contraction of this ring cleaves the cell in two.
• Plant Cells: Plant cells form a cell plate made of membrane and cell wall materials that develops between the separating chromosomes and expands outward to the existing cell membrane.
• Yeast: Budding yeast undergo cytokinesis by converging secretory vesicles at the bud neck between mother and daughter cells.

So the exact start of cytokinesis varies across organisms, but the key event is the physical separation between segregated chromosomes marking the division between two new daughter nuclei.

Why Does Cytokinesis Occur?

Cytokinesis serves the critical purpose of compartmentalizing the genetic material and cytoplasm of the parental cell into two new daughter cells. It acts as the final step of cell division to ensure:

• Partitioning of Cytoplasm – Evenly divides up all the cytoplasm containing organelles and cytoskeletal elements between new cells.
• Nuclear Separation – Completes the isolation of each divided nucleus into one cell.
• Genetic Integrity – Guarantees that both cells receive equivalent and intact genome copies.

Without the compartmentalizing action of cytokinesis, cells would accumulate extra nuclei and DNA content. This could lead to genetic overload, metabolic disruption, and aberrant cell growth.

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What Would Happen Without Cytokinesis?

If cytokinesis fails or does not complete properly, one daughter cell inherits both divided nuclei in a state called binucleation. Additional nuclear divisions without cytokinesis generates multinucleated cells with abnormal DNA content.

Consequences of cytokinesis failure include:

• Polyploidy – Extra copies of the genome disrupts gene regulation.
• Aneuploidy – Uneven chromosome segregation can lead to gains or losses.
• Genetic Instability – Abnormal ploidy promotes mutations and chromosome damage.
• Cell Cycle Disruption – Binucleated cells often exhibit impaired proliferation.
• Cellular Senescence – Multinucleated cells tend to enter irreversible growth arrest.
• Cell Death – Extreme polyploidy and aneuploidy can trigger apoptosis.

Since tetraploid cells contain twice the normal DNA content, they are generally larger in size. When cytokinesis failure occurs in specific cell types, it can have detrimental effects:

• Hepatocytes: Polyploidy contributes to fatty liver disease and cirrhosis.
• Cardiomyocytes: Enlarged heart muscle cells reduce contractile function in cardiomyopathy.
• Neurons: Aneuploid neurons may undergo programmed cell death.
• Cancer Cells: Genomic instability promotes tumor progression.

So the duplication of nuclei without cytokinesis disrupts the stoichiometry of DNA to cytoplasm in cells. This fundamentally alters cell physiology and can lead to tissue dysfunction, especially in sensitive cell types.

When Does Cytokinesis Occur in the Cell Cycle?

Cytokinesis timing is coordinated with mitosis to split replicated DNA content properly into new cells. The sequence of key events is:

1. Prophase – Chromosomes condense and the nuclear envelope breaks down.
2. Prometaphase – Mitotic spindle forms and attaches to chromosomes.
3. Metaphase – Chromosomes align at the metaphase plate.
4. Anaphase – Sister chromatids separate and move poleward.
5. ⇒ Cytokinesis Initiation – Contractile ring assembles at former metaphase plate.
6. Telophase – Daughter nuclei form around segregated chromosomes.
7. ⇒ Cytokinesis Completion – Contractile ring closes and abscission severs cytoplasmic bridge.
8. Interphase – Nuclear envelope reforms as cells enter G1.

So cytokinesis overlaps with the end of mitosis, beginning in late anaphase and finishing in telophase. This ensures the contractile ring bisects the parental cell neatly between segregating chromosomes. If cleavage furrow ingression is blocked with drugs like cytochalasin D, the nuclei continue dividing though cytokinesis fails, resulting in multinucleated cells.

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What Structures Are Involved in Cytokinesis?

The primary cytoskeletal structure driving animal cell cytokinesis is the contractile ring. This dynamic protein complex contains:

Actin Filaments

• Polymerize in a purse-string arrangement around the cell equator.
• Generate contractile force when activated by myosin motor activity.
• Undergo rapid turnover mediated by severing proteins like cofilin.

Myosin II Filaments

• Use ATP hydrolysis to walk along actin filaments.
• Pulling generates contractile force that shrinks the ring.
• Essential for generating cleavage furrow ingression.

Regulatory Proteins

• RhoA – GTPase that promotes actin polymerization and myosin activation.
• Anillin – Bundles actin filaments and links ring to membrane.
• α-actinin – Bundles antiparallel actin filaments to enhance contractility.

Membrane Addition

• Vesiclesderived from Golgi fuse along the ingressing furrow.
• Adds membrane to enable furrow ingression.

So the core cytokinesis apparatus in most animal cells is the contractile actomyosin ring. The coordination of actin and myosin dynamics generates force that, when coupled to vesicle trafficking, can physically divide a cell in two.

How Does the Contractile Ring Assemble?

The assembly and positioning of the contractile ring depends on the mitotic spindle to orient the cell division plane combined with polarity cues to define the cortical division site:

• The mitotic spindle rotates to align perpendicular to the axis of cell division, aligning overlapping microtubules along the cell equator.
• Centralspindlin, a complex of the MKLP1 kinesin and CYK-4 RhoGAP, bundles midzone microtubules and recruits ECT2 RhoGEF.
• ECT2 activates RhoA in a narrow cortical zone marked by anillin, which concentrates myosin and actin assembly factors.
• Broadly distributed factors like formins, profilin, and ARP2/3 nucleate and elongate actin filaments into antiparallel bundles.
• RhoA further stimulates filament assembly while anillin crosslinks actin bundles to form a coherent contractile ring.

So mitotic spindle orientation provides positional information to guide RhoA activation and contractile ring formation precisely where the cell needs to divide. Perturbing this pathway leads to abnormal furrow positioning or complete cytokinesis failure.

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How Does the Contractile Ring Constrict the Cell?

The contractile ring divides the cell through a mechanochemical process coupling actomyosin-based contraction with membrane trafficking:

• Nonmuscle myosin II motors walk along antiparallel actin filament bundles, sliding filaments to generate contractile force.
• The actin cytoskeleton is anchored to the plasma membrane via linker proteins like anillin.
• As myosin contracts the ring, the actin filaments pull the anchored membrane inward.
• This forms an ingressing cleavage furrow, but membrane addition is required to allow furrow ingression.
• Vesicle fusion inserts new membrane along the furrow, expanding the surface area.
• Abscission finally severs the thin intracellular bridge to complete division.

Contractile force alone can only reduce ring circumference by about 10% before filament densities become too high. Thus membrane trafficking is essential to support the dramatic shape changes of cell division.

What Controls Timing of Cytokinesis?

Proper timing of cytokinesis is critical to avoid separating chromosomes prematurely before they have fully segregated to opposite poles:

• The mitotic checkpoint inhibits cytokinesis until all kinetochores are properly attached to spindle microtubules.
• Unattached kinetochores activate the spindle assembly checkpoint, blocking anaphase onset and contractile ring assembly.
• Once chromosomes successfully biorient on the metaphase plate, the checkpoint is satisfied allowing mitotic progression.
• Anaphase spindle elongation then stimulates RhoA activation to initiate furrowing only after sister chromatids have started separating.
• The centralspindlin complex clusters at the spindle midzone to inhibit RhoA until late anaphase, preventing premature ingression.

So satisfaction of the spindle checkpoint couples chromosome segregation in anaphase with initiation of cytokinesis. The mechanisms preventing furrow ingression before anaphase help protect genetic integrity by avoiding premature cell division across unseparated sister chromatids.

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What Happens When Cytokinesis Fails?

Cytokinesis failure generates tetraploid cells with extra centrosomes that exhibit chromosome instability and disrupted proliferation:

• Actomyosin ring defects cause failed initiation or incomplete ingression.
• Weakening of microtubule bundles impairs central spindle-mediated RhoA activation.
• Loss of key structural proteins like anillin, RhoA, or myosin II prevents contractile ring formation.
• Insufficient membrane addition inhibits furrow ingression and abscission.
• DNA damage and chromatin bridges can physically obstruct the cleavage furrow.
• Merotely, with single kinetochores attached to both spindle poles, distorts furrow positioning.
• Cell adhesion or cortical rigidity impedes deformation of cell shape during division.

Since tetraploid cells contain twice the normal DNA content, they are more prone to acquiring mutations that promote tumorigenesis. Failed cytokinesis also generates chromosome instability that evolves tumors toward higher malignancy.

Conclusion

In summary, cytokinesis partitions the duplicated DNA content and cytoplasm of a parental cell into two genetically identical daughter cells at the end of mitosis. It depends on an actomyosin contractile ring that couples force generation with membrane trafficking to divide a cell in two. Temporal coordination with chromosome segregation ensures the genetic integrity of new cells. Failed cytokinesis generates tetraploid cells with abnormal ploidy that disrupts proliferation control and genome stability, making it a critical process for maintaining healthy tissues.

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