During cytokinesis, the cytoplasm is what’s actually dividing. That includes everything outside the nucleus: the fluid interior of the cell (cytosol), all the organelles floating in it (mitochondria, endoplasmic reticulum, Golgi apparatus), and the plasma membrane itself. The chromosomes have already been separated during the earlier stages of mitosis. Cytokinesis is the physical split of one cell body into two, parceling out all the remaining cellular machinery so each daughter cell can function independently.
The Cytoplasm Is the Target, Not the Nucleus
This distinction trips people up because mitosis and cytokinesis are often taught as one continuous process, but they’re doing very different jobs. Mitosis divides the genetic material. Cytokinesis divides the physical cell. By the time cytokinesis begins, the two sets of chromosomes have already migrated to opposite poles of the cell. What remains is a single bag of cytoplasm that needs to become two separate, membrane-enclosed cells.
That means cytokinesis has to split the cytosol, distribute organelles to both sides, and generate enough new plasma membrane to seal off two independent cells. The way this happens differs dramatically between animal and plant cells, but the goal is the same: divide the cytoplasm and everything in it.
How Animal Cells Pinch in Two
Animal cells divide from the outside in. A structure called the contractile ring assembles just beneath the plasma membrane at the cell’s equator, forming a belt around the middle of the cell. This ring is built from two key protein filaments: actin (the same structural protein that gives cells their shape) and myosin II (a motor protein also found in muscle). When myosin pulls on actin, the ring tightens like a drawstring on a bag, squeezing the cell inward to create what’s called the cleavage furrow.
The organization is strikingly similar to how muscle contracts. The actin filaments run parallel to the ring with mixed orientations, and bipolar myosin filaments slide between them. In some cell types, the arrangement even forms a repeating striped pattern reminiscent of muscle fibers. Bundling proteins hold the filaments together and anchor them to the plasma membrane, ensuring the force is directed inward.
As the ring tightens, the cell needs more surface area to cover two cells instead of one. To solve this, intracellular vesicles (small membrane-bound packets) fuse with the plasma membrane near the furrow, adding new membrane material in real time. Without this membrane addition, the cell would simply run out of surface to close off both daughter cells.
How Plant Cells Build a Wall Between Daughters
Plant cells can’t pinch inward because they’re encased in a rigid cell wall. Instead, they divide from the inside out by constructing a brand-new wall between the two daughter nuclei.
The process centers on a structure called the phragmoplast, a cylindrical scaffold made of microtubules and actin filaments arranged in two opposing arrays with their growing ends pointed toward the center. This scaffold acts as a highway system: motor proteins carry small vesicles produced by the Golgi apparatus along the microtubule tracks to the middle of the cell. There, the vesicles fuse with each other to form a flat, expanding disc called the cell plate.
The cell plate starts at the center and grows outward toward the existing cell walls. As it expands, the phragmoplast disassembles behind the growing edge and rebuilds in front of it, continuously shuttling new vesicles to wherever construction is happening. Specialized tethering factors and fusion proteins coordinate the merging of vesicles. Eventually the cell plate reaches the outer walls, fuses with them, and becomes the new cell wall separating the two daughter cells.
Organelles Get Sorted Before the Split
Dividing the cytosol is straightforward since it’s just fluid. Organelles are a different challenge. Each daughter cell needs its own supply of mitochondria, endoplasmic reticulum (ER), Golgi apparatus, endosomes, and peroxisomes to survive.
The cell handles this through a combination of fragmentation and redistribution that begins well before cytokinesis starts. During earlier mitotic stages, the Golgi apparatus breaks apart into small vesicles and tubular clusters that scatter throughout the cell. The ER undergoes significant structural changes, shifting from its usual network shape. Mitochondria undergo fission, splitting into smaller units that spread more evenly across both halves of the cell. Endosomes and peroxisomes are similarly separated and redistributed.
By the time the cleavage furrow or cell plate actually bisects the cytoplasm, most organelles are already positioned so that roughly equal numbers end up on each side. Completing the final split specifically requires mitochondrial fission and endosome trafficking, ensuring neither daughter cell is shortchanged on energy-producing or membrane-recycling machinery.
The Signal That Tells the Cell Where to Divide
The cell doesn’t just split anywhere. A signaling protein called RhoA determines the exact position of the division plane in animal cells. At the onset of anaphase (when chromosomes start separating), RhoA becomes active in a narrow zone along the equatorial cell cortex, precisely between the two groups of separating chromosomes.
Once activated in that strip, RhoA triggers two things simultaneously. It switches on formins, which are proteins that build the long, straight actin filaments needed for the contractile ring. And it activates a kinase called ROCK, which turns on myosin II motor activity. This two-pronged activation ensures that actin filaments polymerize and myosin starts pulling on them only at the correct location. Premature actin assembly is prevented because formins stay locked in an inactive state until RhoA physically binds and releases them.
RhoA also recruits scaffold proteins like anillin and septins to the division site. Septins are particularly important because they form structures that act as diffusion barriers, compartmentalizing the membrane at the furrow and preventing the ring’s components from drifting away. In yeast, septin rings also recruit the machinery responsible for the final membrane cut.
How the Last Bridge Gets Cut
Even after the contractile ring has fully tightened, the two daughter cells remain connected by a thin tube called the intercellular bridge. For a long time, scientists assumed this bridge simply snapped under mechanical tension. That turned out to be wrong.
The actual severing is performed by a membrane-remodeling complex called ESCRT-III, the same molecular machinery cells use for other membrane-cutting tasks like sorting cargo inside compartments and budding certain viruses from the cell surface. ESCRT-III components assemble at a structure in the middle of the bridge called the midbody, then move to one side and polymerize into filaments that constrict the remaining membrane tube. This constriction narrows the bridge until the membrane fuses shut, completing a process called abscission.
This final step is the true point of no return. Once abscission occurs, the two daughter cells are physically independent, each with its own complete plasma membrane, its own set of organelles, and its own copy of the genome. Cytokinesis is complete.
When Cytokinesis Doesn’t Happen
Sometimes cells deliberately skip cytokinesis. The nucleus divides, but the cytoplasm doesn’t split, producing a single cell with multiple nuclei. These multinucleated cells are called coenocytes (when nuclei multiply without cytoplasmic division) or syncytia (when separate cells fuse together).
This isn’t always a mistake. Human skeletal muscle fibers are syncytia containing hundreds of nuclei, which helps coordinate protein production across very long cells. Certain placental tissues in animals use coenocytic growth to form large nutrient-transferring structures. In some organisms like slime molds, the entire body is essentially one giant coenocytic cell. These examples show that cytokinesis is not an inevitable consequence of nuclear division. It’s a regulated event that cells can control, skip, or modify depending on what the tissue needs.