Mitosis has five stages: prophase, prometaphase, metaphase, anaphase, and telophase. The entire process takes roughly 30 to 60 minutes in a typical mammalian cell, though most of that time is spent in the earlier stages. Each stage accomplishes a specific mechanical task, building toward the moment when one cell splits its duplicated chromosomes into two identical sets. Here’s what happens at each step.
Prophase: Packaging the DNA
Before a cell can divide, it needs to take the long, tangled strands of DNA scattered throughout its nucleus and compress them into compact, manageable units. That’s what prophase accomplishes. Specialized protein complexes called condensins wind the DNA into tightly coiled chromosomes, shortening each strand by a factor of roughly 10,000. Condensins also untangle sections of DNA that have become knotted around each other, which prevents the strands from ripping apart later when they’re pulled to opposite sides of the cell.
While the chromosomes are condensing, two small structures called centrosomes begin migrating to opposite ends of the cell. These centrosomes act as anchor points, and they start assembling a network of protein filaments (microtubules) that will eventually form the mitotic spindle. By the end of prophase, you can see distinct X-shaped chromosomes under a microscope, each consisting of two identical copies (sister chromatids) joined at a pinch point called the centromere.
Prometaphase: Breaking Open the Nucleus
Prometaphase begins when the membrane surrounding the nucleus breaks apart. An enzyme triggers this by chemically modifying the proteins that form the nuclear envelope’s inner scaffolding, causing that scaffolding to disassemble. The membrane then fragments into tiny bubble-like vesicles that scatter into the surrounding cell fluid. These vesicles aren’t destroyed. They’ll be recycled later to build new nuclear envelopes in the daughter cells.
With the nuclear barrier gone, spindle microtubules can now reach the chromosomes. Each chromosome has a specialized docking site on its centromere called a kinetochore, a complex of proteins designed to grab and hold onto microtubules. The initial contact is somewhat random: a microtubule extending from one centrosome brushes against a kinetochore and latches on. Motor proteins at the kinetochore then pull the chromosome toward that centrosome, while the growing microtubules simultaneously push it away. This creates a tug-of-war that causes chromosomes to shuffle back and forth across the cell, a hallmark of prometaphase visible under time-lapse microscopy.
Metaphase: Lining Up at the Center
Metaphase is the alignment phase. Each chromosome must achieve “bi-orientation,” meaning one sister chromatid is connected to microtubules from one centrosome while the other sister is connected to microtubules from the opposite centrosome. When this happens, the balanced pulling forces position the chromosome precisely at the cell’s midline, forming what’s called the metaphase plate.
Getting every chromosome bi-oriented is critical, and the cell has a quality-control system to make sure it happens correctly. If a kinetochore is unattached or both sisters accidentally connect to the same centrosome (a common early error), the cell activates what’s known as the spindle assembly checkpoint. This checkpoint blocks the cell from advancing to the next stage until the mistake is fixed. An error-correction enzyme at the centromere detects attachments that aren’t generating proper tension between the two sisters. It destabilizes those incorrect connections so the kinetochore can try again, giving the chromosome another chance to attach to the right pole. Only when every single chromosome is properly bi-oriented and under tension does the checkpoint release its brake.
Anaphase: Pulling the Chromosomes Apart
Anaphase is the shortest and most dramatic stage. It begins the instant the spindle assembly checkpoint is satisfied, which triggers the destruction of the proteins holding sister chromatids together. The two halves of each chromosome separate simultaneously across the entire cell.
Chromosome movement during anaphase happens through two distinct mechanisms that work at the same time. In the first (anaphase A), the microtubules connecting kinetochores to centrosomes shorten by disassembling at their ends, reeling the separated chromatids toward opposite poles. In the second (anaphase B), the spindle itself elongates. Microtubules from opposite poles slide past each other and push the two centrosomes farther apart, while additional pulling forces from the cell’s outer edge tug the poles outward. Together, these two mechanisms ensure the chromosome sets end up well separated.
The trigger for anaphase is also what eventually ends mitosis. Destruction of a key regulatory protein called cyclin B1 inactivates the enzyme complex that drove the cell into mitosis in the first place. Cyclin B1 levels build steadily in the hours before division, peaking at metaphase, then drop sharply as the protein is tagged for rapid destruction. Without it, the molecular machinery of mitosis winds down.
Telophase: Rebuilding Two Nuclei
Once the chromosomes arrive at opposite poles, the cell begins reversing many of the changes it made during prophase. The chromosomes start to decondense, loosening back into the extended form needed for reading genes. More importantly, new nuclear envelopes form around each set of chromosomes. This reassembly follows a specific order: vesicles derived from the inner nuclear membrane attach to the chromosome surfaces first, beginning as early as late anaphase. Pore complexes and the structural scaffolding of the nucleus are added afterward, during telophase and into cytokinesis.
Telophase overlaps with cytokinesis, the physical division of the cell itself. In animal cells, a ring of protein filaments assembles just beneath the cell membrane at the equator. This contractile ring tightens like a drawstring, pinching the cell inward until it splits into two separate daughter cells, each with its own nucleus and a complete copy of the genome.
What Drives the Whole Process
A single enzyme complex acts as mitosis’s master switch. It consists of a protein called cyclin B1 paired with an activating partner. Cyclin B1 levels begin rising during DNA replication and continue climbing through the preparation phase before division. By late in that preparation phase, about 70 to 80 percent of cyclin B1 molecules are bound to their activating partner, compared to only 30 to 40 percent earlier. This sharp increase in active complex is what pushes the cell over the threshold into mitosis. The complex then drives nuclear envelope breakdown, chromosome condensation, and spindle assembly by chemically modifying dozens of target proteins throughout the cell.
Destroying cyclin B1 at the metaphase-to-anaphase transition is equally important. Cells that can’t degrade it remain stuck in a mitotic state, unable to decondense chromosomes or rebuild their nuclei.
When Mitosis Goes Wrong
Errors during mitosis can leave daughter cells with the wrong number of chromosomes, a condition called aneuploidy. This happens most often when the spindle assembly checkpoint fails to catch an improper attachment, allowing a chromosome to travel to the wrong pole during anaphase.
The consequences depend on which chromosomes are affected and which cell type is dividing. In developing embryos, gaining an extra copy of chromosome 21 produces Down syndrome. People with Down syndrome frequently develop Alzheimer’s disease by age 40, likely because chromosome 21 carries genes involved in that neurodegenerative process. Errors in other chromosomes are usually lethal to the embryo.
In adults, mitotic errors in body cells are a hallmark of cancer. Chromosomal instability, the tendency to gain or lose chromosomes during division, characterizes aggressive tumors and drives resistance to chemotherapy. Breast cancer metastases, for example, often arise from subpopulations of cells with unstable chromosome numbers. Even outside of cancer, reduced function of spindle checkpoint proteins leads to progressive aneuploidy across tissues, accelerating age-related problems like muscle wasting, cataracts, impaired wound healing, and brain degeneration.
Open vs. Closed Mitosis
The stages described above apply to animal and plant cells, which undergo “open” mitosis, meaning the nuclear envelope fully disassembles. Not all organisms do this. Most fungi keep their nuclear envelope intact throughout division, carrying out “closed” mitosis with the spindle forming entirely inside the nucleus. Some single-celled organisms, like certain dinoflagellates, divide without disassembling their nuclear envelope and without even building a traditional spindle inside. These variations are a reminder that mitosis, while fundamentally conserved, has been adapted in different ways across the tree of life.