The Cytokinetic Contractile Ring

Core Concept

Cytokinesis — the physical division of one cell into two — is driven in animal cells by a contractile ring of actin filaments and myosin II assembled just beneath the plasma membrane at the cell equator. The ring uses the same sliding-filament machinery as muscle: myosin II pulls antiparallel actin filaments together, tightening the ring like a purse string and pinching the cell into two daughter cells. Ring formation is spatially controlled by the mitotic spindle (via RhoA signaling) so that division occurs precisely between the two sets of chromosomes.

Key Components

• Contractile ring: a circumferential band of actin filaments and myosin II under the membrane.
• Myosin II: the motor that generates contractile force by sliding actin filaments.
• Formins (mDia): nucleate and elongate the unbranched actin filaments of the ring.
• RhoA GTPase: the master regulator that activates formins and myosin at the equator.
• Centralspindlin / Ect2: the spindle-derived complex that recruits and activates RhoA at the equatorial cortex.
• Anillin and septins: scaffold proteins that link the ring to the plasma membrane.
• Cleavage furrow: the ingressing membrane constriction produced by the ring.

Mechanism / How It Works

1. Positioning: in anaphase, the spindle's central region (via centralspindlin and the GEF Ect2) establishes a band of active RhoA at the equatorial cortex.
2. Assembly: active RhoA stimulates formins to nucleate unbranched actin filaments and activates myosin II, assembling the contractile ring beneath the membrane.
3. Constriction: myosin II cross-bridges slide antiparallel actin filaments past one another, and the ring tightens — the "purse-string" constriction that ingresses the cleavage furrow.
4. Disassembly (tandem with constriction): as the ring shrinks, actin filaments are simultaneously disassembled (depolymerized) so the ring can keep constricting without thickening.
5. Abscission: when the furrow closes down to a narrow intercellular bridge, the membranes are finally severed (abscission by the ESCRT machinery), yielding two daughter cells.
6. Plant variant: plants build a phragmoplast — a scaffold that directs vesicles to fuse into a new cell plate at the division plane — because a rigid cell wall prevents purse-string constriction.

Energy and Directionality

Cytokinesis is ATP/GTP-driven and vectorial (ring tightens inward). Myosin II hydrolyzes ATP to slide actin filaments (contraction), RhoA cycles GTP (spatial switch), and formins and actin turnover consume ATP/GTP as the ring assembles and disassembles. The direction of constriction — inward, at the equator — is set by the equatorial localization of RhoA, itself dictated by spindle geometry, ensuring the furrow forms exactly between the separated chromosomes.

Experimental Evidence / Technique

• Live-cell imaging of the ring: fluorescent actin and myosin II reveal a contracting ring at the equator whose constriction rate matches the rate of actin disassembly.
• Drug perturbations: latrunculin (actin depolymerization) or blebbistatin (myosin II inhibition) block cytokinesis, proving both actin and myosin II are required.
• RhoA manipulations: local RhoA activation anywhere on the cortex induces an ectopic furrow; RhoA inhibition prevents cytokinesis — demonstrating RhoA is the spatial switch.
• Laser microsurgery: relocating or destroying a mitotic spindle repositions the furrow, showing the spindle (via its central region) dictates ring position.
• Caenorhabditis elegans / fly genetics: mutants in myosin II, formins, or RhoA effectors fail cytokinesis and become multinucleate.

How it works

1. Positioning: in anaphase, the spindle's central region (via centralspindlin and the GEF Ect2) establishes a band of active RhoA at the equatorial cortex.
2. Assembly: active RhoA stimulates formins to nucleate unbranched actin filaments and activates myosin II, assembling the contractile ring beneath the membrane.
3. Constriction: myosin II cross-bridges slide antiparallel actin filaments past one another, and the ring tightens — the "purse-string" constriction that ingresses the cleavage furrow.
4. Disassembly (tandem with constriction): as the ring shrinks, actin filaments are simultaneously disassembled (depolymerized) so the ring can keep constricting without thickening.
5. Abscission: when the furrow closes down to a narrow intercellular bridge, the membranes are finally severed (abscission by the ESCRT machinery), yielding two daughter cells.
6. Plant variant: plants build a phragmoplast — a scaffold that directs vesicles to fuse into a new cell plate at the division plane — because a rigid cell wall prevents purse-string constriction.

Common confusions

• "The contractile ring is made of microtubules." It is actin + myosin II; microtubules (the spindle) position the ring but do not constrict it.
• "The ring contracts like a rubber band." Unlike rubber, the ring disassembles as it constricts — it is a dynamic, turning-over structure, not a passive elastic band.
• "Cytokinesis and mitosis are the same thing." Mitosis divides the nucleus; cytokinesis divides the cytoplasm. They can be uncoupled (e.g. multinucleate cells).
• "Plant and animal cells divide the same way." Plants build a cell plate (phragmoplast) because the cell wall prevents purse-string constriction.
• "Anywhere on the membrane can form a furrow." Furrow position is tightly specified by the spindle via RhoA at the equator.

Quick review

• Contractile ring = actin + myosin II at the equatorial cortex.
• RhoA (activated by spindle/centralspindlin/Ect2) positions and assembles the ring.
• Formins nucleate actin; myosin II slides filaments → constriction; ring disassembles as it tightens.
• Abscission (ESCRT) completes division.
• Plants use the phragmoplast/cell plate instead.