Mitosis is the process by which a single cell copies its chromosomes and divides them equally into two genetically identical daughter cells. The entire process typically takes 30 to 60 minutes, a small fraction of the total cell cycle, since cells spend most of their time in interphase (the growth period between divisions), which lasts anywhere from about 6 hours to much longer depending on the cell type. Mitosis is how your body grows new tissue, replaces worn-out cells, and repairs damage. Every daughter cell ends up with the same complete set of chromosomes as the original.
What Happens Before Mitosis Begins
Before a cell enters mitosis, it goes through interphase, where it grows, carries out its normal functions, and, crucially, makes a complete copy of every chromosome. By the time interphase ends, each chromosome exists as two identical copies called sister chromatids, joined together at a connection point. The cell has also duplicated its centrosomes, the structures that will later organize the machinery for pulling chromosomes apart. Think of interphase as the preparation stage: the cell won’t divide until everything has been copied and checked.
Prophase: Chromosomes Take Shape
The first visible sign that mitosis has begun is the appearance of distinct chromosomes. During interphase, DNA exists in a loose, spread-out form. In prophase, protein complexes called condensins wrap the DNA tightly around itself, compacting it into the short, thick structures you’d recognize from a textbook image. Each chromosome is visibly made of its two sister chromatids joined together.
While the chromosomes condense, the two centrosomes migrate to opposite sides of the cell. They begin assembling the mitotic spindle, a network of protein filaments (microtubules) that will eventually grab the chromosomes and move them. By late prophase, the membrane surrounding the nucleus starts to break down, giving the spindle access to the chromosomes inside.
Metaphase: Lining Up at the Center
During metaphase, spindle fibers attach to each chromosome at a specialized protein structure called the kinetochore. Each sister chromatid has its own kinetochore, and fibers from opposite poles of the spindle connect to opposite chromatids. This tug-of-war from both sides pulls every chromosome to the exact center of the cell, forming what’s called the metaphase plate.
The central positioning of the metaphase plate isn’t just cosmetic. It ensures the cell divides symmetrically into two equal-sized daughters. If chromosomes are off-center, the connections between kinetochores and spindle fibers become unstable, and a safety mechanism called the spindle assembly checkpoint kicks in. This checkpoint delays the next phase until every single chromosome is properly attached and aligned. When chromosomes are experimentally pushed off-center, they relocate to the middle before division proceeds, and the checkpoint is what buys the cell enough time to make that correction. If the checkpoint is bypassed too early, the cell divides unevenly, producing daughter cells of different sizes.
Anaphase: Pulling the Copies Apart
Anaphase is the dramatic moment when the sister chromatids are physically separated. Throughout earlier stages, a ring-shaped protein complex called cohesin holds each pair of sister chromatids together. At the start of anaphase, an enzyme cleaves the cohesin ring, releasing the two chromatids from each other. Once freed, motor proteins along the spindle fibers reel each chromatid toward opposite poles of the cell.
The timing of this separation is tightly controlled. The spindle assembly checkpoint blocks anaphase by preventing the activation of the molecular machinery that would destroy cohesin’s protective factors. Only when every chromosome is correctly attached and under tension does the checkpoint switch off, allowing the cohesin-cutting enzyme to do its work. This all-or-nothing approach means that either all chromosomes separate simultaneously or none do.
Telophase: Rebuilding Two Nuclei
Once the separated chromatids arrive at opposite poles, the cell begins reversing many of the changes from prophase. The chromosomes decondense, loosening back into their spread-out interphase form. A new nuclear envelope assembles around each set of chromosomes, creating two distinct nuclei within a single cell. The spindle fibers disassemble, having completed their job.
Cytokinesis: Splitting the Cell in Two
Telophase overlaps with cytokinesis, the physical division of the cytoplasm. In animal cells, a band of actin filaments and the motor protein myosin gathers around the cell’s equator, forming what’s called a contractile ring. This ring squeezes inward like a drawstring, pinching the cell membrane into a deepening groove called the cleavage furrow. The furrow eventually pinches all the way through, producing two separate daughter cells, each with its own nucleus and roughly equal share of the cytoplasm and organelles.
Disrupting the actin-myosin system (with drugs or genetic manipulation) results in incomplete or failed cytokinesis, leaving cells with two nuclei stuck in one body. Plant cells handle this step differently, building a new cell wall between the two daughter nuclei rather than pinching inward, but the end result is the same: two independent cells.
How Mitosis Differs From Meiosis
Mitosis produces two cells that are genetically identical to each other and to the parent cell. Each daughter cell is diploid, meaning it has the full set of chromosomes (46 in humans). Meiosis, by contrast, is used only to produce sex cells (eggs and sperm). It involves two rounds of division and produces four cells, each with half the chromosome count. Meiosis also shuffles genetic material between chromosomes, introducing variation. Mitosis does neither of these things. Its purpose is precise duplication, not diversity.
What Goes Wrong When Mitosis Fails
When chromosomes don’t separate correctly during mitosis, daughter cells end up with too many or too few chromosomes, a condition called aneuploidy. Nearly 70% of solid human tumors are aneuploid, making chromosome missegregation one of the most common features of cancer. Errors in mitosis don’t just change chromosome number. They also cause structural damage like deletions, duplications, and rearrangements of chromosome segments.
The relationship between mitotic errors and cancer is nuanced. Low rates of chromosome missegregation can promote tumor growth, especially when the cell’s usual safeguards against abnormal chromosome counts have been disabled. But very high rates of segregation errors are actually toxic to tumors, because cells lose chromosomes essential for survival. Recent research also shows that cells with severely abnormal chromosome sets can trigger an immune response, raising the possibility that the body sometimes recognizes and attacks these defective cells on its own.
Outside of cancer, mitotic errors during early embryonic development are almost universally lethal. Trisomy 21 (Down syndrome), where cells carry an extra copy of chromosome 21, is one of the very few survivable examples of a whole-chromosome error in humans.