During cytokinesis, a cell physically splits into two daughter cells after its chromosomes have already been copied and separated. This is the final act of cell division, occurring at the end of mitosis, and it involves pinching or building a barrier through the middle of the cell so each daughter gets its own complete set of contents. The process differs significantly between animal and plant cells, but the goal is the same: two independent, functional cells where there was one.
Where Cytokinesis Fits in Cell Division
Cytokinesis begins during the later stages of mitosis, typically starting in anaphase (when chromosomes are moving to opposite poles) and finishing during or after telophase. It overlaps with nuclear division rather than waiting for it to fully complete. The M phase of the cell cycle includes both mitosis and cytokinesis together, though they are distinct processes. Mitosis divides the nucleus; cytokinesis divides everything else.
How the Cell Knows Where to Split
The position of the division isn’t random. The mitotic spindle, the structure that pulled the chromosomes apart, also tells the cell exactly where to cut. Research in early embryos has shown this happens through two consecutive signals. First, the star-shaped clusters of protein fibers radiating from the spindle poles (called asters) establish a rough position for the split. Then a second signal from the midzone, the bundle of fibers running between the two groups of separated chromosomes, refines that position. The result is a division plane that bisects the cell right between the two new chromosome sets, producing two equal daughter cells.
The Contractile Ring in Animal Cells
In animal cells, cytokinesis works by squeezing. A band of protein filaments assembles just beneath the cell membrane at the division site. This contractile ring is built primarily from actin filaments and motor proteins called myosin-II. Myosin-II grabs onto the actin filaments and pulls them, generating tension the same way muscle fibers contract. As the ring tightens, it pulls the membrane inward, creating a visible groove around the cell’s equator called the cleavage furrow.
The assembly of this ring is triggered by a signaling protein called RhoA, which becomes active in a narrow zone at the future division site. RhoA essentially flips the switch that tells actin and myosin to organize into a functional, tension-generating bundle at precisely the right location. Without this signal, the ring components float around the cell without assembling into anything useful.
The cleavage furrow deepens progressively, like tightening a drawstring on a bag, until the cell is pinched into two connected spheres joined by a thin bridge.
The Final Cut: Abscission
That thin bridge connecting the two nearly separated cells doesn’t just snap. It contains a dense structure called the midbody, and severing it requires dedicated molecular machinery. A group of 12 related proteins called the ESCRT-III complex forms spiral filaments that constrict the remaining membrane bridge and cut it, completing the separation. Additional enzymes localize to the midbody bridge through interactions with ESCRT-III partners to carry out this final scission.
Cells also have a safety checkpoint here. If chromosomes are caught in the bridge or haven’t fully cleared the division site, an “abscission checkpoint” delays the final cut to prevent damage. Only when everything is clear does the cell commit to the split.
Plant Cells Build a Wall Instead
Plant cells can’t pinch inward because they’re surrounded by a rigid cell wall. Instead of squeezing, they build a new wall from the inside out. A structure called the phragmoplast, made of protein fibers oriented between the two new nuclei, guides the process. Small vesicles produced by the Golgi apparatus (the cell’s packaging center) are delivered along these fibers to the middle of the cell.
These vesicles are squeezed into dumbbell-shaped structures that fuse together at their ends, creating a honeycomb-like network of tubes and membranes called the cell plate. This structure expands outward from the center of the cell toward the existing cell walls on all sides. Once the cell plate reaches and fuses with the outer membrane, the two daughter cells are fully walled off from each other. New cell wall material is then deposited to strengthen the partition.
How Organelles Get Divided
Splitting the chromosomes and cytoplasm is only part of the job. Each daughter cell also needs a working set of organelles, and the cell has specific strategies for distributing them.
Mitochondria, which generate the cell’s energy, undergo a dramatic reorganization. Upon entry into mitosis, the normally interconnected mitochondrial network fragments into smaller pieces that disperse evenly throughout the cytoplasm. During cytokinesis, these fragments are actively recruited to the cleavage furrow, where they remain until division is complete. If the machinery responsible for mitochondrial fragmentation is disrupted, cells can’t distribute mitochondria evenly, and cytokinesis itself often fails.
The endoplasmic reticulum, a sprawling membrane network involved in protein and lipid production, splits into two large pools of membranes during early mitosis. These pools maintain their structure throughout division and are reorganized into complete networks in each daughter cell after the chromosomes have separated. The nuclear envelope, which broke down at the start of mitosis, reassembles around each new set of chromosomes during this same window.
What Happens When Cytokinesis Fails
When the physical split doesn’t happen, the result is a single cell with two nuclei and double the normal number of chromosomes. These tetraploid cells are genetically unstable. They contain extra copies of centrosomes (the structures that organize the spindle), which can cause chromosomes to be pulled in three or four directions during the next division instead of two. This generates cells with wildly abnormal chromosome counts, a hallmark of many cancers.
Healthy cells have a defense against this. When cytokinesis fails, the extra centrosomes trigger a tumor suppressor pathway that stabilizes p53, a protein often called the “guardian of the genome.” Activated p53 halts cell growth, preventing the dangerous tetraploid cell from dividing further. This arrest after cytokinesis failure was first observed in 1967 and has since been identified as one of the body’s key defenses against tumor formation.
Defects in mitosis and cytokinesis are considered the most common routes by which potentially cancerous tetraploid cells arise in the body. When the p53 safety mechanism is itself mutated or disabled, these cells can continue to proliferate. Tetraploid cells are capable of promoting tumor growth regardless of how they originally formed, making cytokinesis failure a significant early event in cancer development.