How many divisions occur during meiosis?

Meiosis involves exactly two cell divisions, called meiosis I and meiosis II. A single cell with a full set of chromosomes enters the process and, after those two back-to-back divisions, produces four cells that each carry half the original chromosome count. Those half-loaded cells are the precursors to sperm and eggs, and the reason you inherit one copy of each chromosome from each parent rather than a doubled-up mess. The two-division structure is what makes sexual reproduction possible, but the way those divisions play out is more layered than a simple count suggests.

What the Two Divisions Actually Do

The two rounds of meiosis have fundamentally different jobs. Meiosis I is the “reductional” division: it separates pairs of matching chromosomes (one from your mother, one from your father) so that each resulting cell gets just one member of each pair. Meiosis II is the “equational” division: it splits the two identical copies of each chromosome apart, much like an ordinary cell division does. A crucial detail is that there is no DNA replication between the two rounds. The cell copies its DNA once, before meiosis I begins, and then divides twice in a row without copying again. That is how the chromosome number gets cut in half.

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Each of the two divisions passes through the same four stages: prophase, metaphase, anaphase, and telophase. So if you count individual stages, there are eight in total across the full process. But the stages are not identical between the two rounds. Prophase of meiosis I is unusually long and elaborate. During it, matching chromosomes find each other, line up side by side, and physically swap segments of DNA, a process called crossing over. That swapping is the main engine of genetic shuffling. By the time the cell reaches meiosis II, most of the interesting genetic rearrangement is already done, and the second division proceeds relatively quickly.

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Why Two Divisions Instead of One

A reasonable question is why the cell bothers with two separate divisions rather than achieving the same result in a single step. The answer has to do with how chromosomes are physically organized. Before meiosis begins, the cell replicates its DNA, so every chromosome exists as a pair of joined identical copies (sister chromatids). Meiosis I pulls apart the matched pairs of different chromosomes (homologs), while meiosis II pulls apart those joined identical copies. Trying to do both jobs in a single division would require the cell to simultaneously recognize two completely different kinds of chromosome relationships and sort them correctly. Splitting the task into two rounds lets the machinery focus on one sorting problem at a time.

Making this work requires precise molecular coordination between the two divisions. During meiosis I, the identical copies of each chromosome must stay glued together at their center point (the centromere), even as everything else around them is being pulled apart. A protein called shugoshin acts as a guardian at the centromere, physically shielding the molecular glue from being cut too early. Only after meiosis I is complete does that protection get removed, allowing the second division to separate the identical copies.

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The name “shugoshin” comes from the Japanese word for “guardian spirit,” which gives you a sense of how central this protein’s protective role is. Without it, the glue holding identical copies together would be destroyed during the first division, and the second division would have nothing left to separate. Cells missing shugoshin activity lose chromosomes at alarming rates during meiosis.

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How the Two Divisions Compare to Ordinary Cell Division

Ordinary cell division (mitosis) involves just one division and produces two cells that are genetic copies of the original. Meiosis, with its two divisions, yields four cells that are genetically distinct from one another and from the parent cell. That difference in output is the whole point: mitosis is for growth and repair, meiosis is for producing sex cells.

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The second meiotic division closely resembles mitosis in its mechanics. Sister chromatids line up, the cell pulls them to opposite sides, and the cell splits. Researchers sometimes describe meiosis II as “mitosis-like” for this reason. What makes meiosis II different from actual mitosis is context: the cell entering meiosis II already has half the normal chromosome number, so the products end up haploid rather than diploid. The heavy lifting for genetic diversity happens during meiosis I, especially during that long prophase when chromosomes swap segments. Meiosis II is essentially the cleanup crew.

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Meiosis in Sperm Versus Eggs

Both sperm and egg cells go through the same two meiotic divisions, but the process looks remarkably different in practice. In sperm production, the two divisions are symmetric: one cell becomes two, then two become four, and all four mature into functional sperm. The whole process takes roughly two to three months in humans and runs continuously from puberty onward.

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Egg production is strikingly asymmetric. Each division produces one large cell that retains almost all the cytoplasm and one tiny cell (a polar body) that is essentially discarded. So although two divisions technically yield four cells, only one of them becomes a viable egg. The other three are polar bodies that degenerate. This unequal splitting ensures the future egg is packed with enough cellular material to support the early stages of embryonic development.

The timing is also dramatically different. In human females, egg cells enter meiosis I during fetal development and then stall partway through the first division, during the diplotene stage of prophase I. They can remain frozen in that state for decades. Meiosis I doesn’t resume until ovulation, meaning an egg ovulated at age 35 has been sitting in arrested meiosis for roughly 35 years. Meiosis II then begins but pauses again, completing only if the egg is fertilized.

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When the Divisions Go Wrong

Errors during meiosis are surprisingly common, and the consequences vary depending on which of the two divisions misfires. The most frequent problem is nondisjunction, where chromosomes fail to separate properly and one daughter cell ends up with an extra chromosome while the other is missing one. Research on preimplantation embryos has found that error rates during meiosis I and meiosis II are comparable in frequency, but they tend to produce different kinds of mistakes. Meiosis I errors more often result in extra chromosome material in the egg, while meiosis II errors lead to a more random mix of extra and missing chromosomes.

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These errors have real clinical significance. An extra copy of chromosome 21, for instance, causes Down syndrome. Most chromosomal abnormalities that arise from meiotic errors are severe enough that embryos carrying them do not survive, which is one reason early miscarriage rates are high. Only a handful of trisomies (an extra chromosome) are compatible with live birth.

Why Maternal Age Matters

The long arrest period in egg cells creates a vulnerability that worsens with age. Because an egg can sit paused in meiosis I for decades, the molecular structures holding chromosomes in place gradually degrade. A study comparing oocytes from younger and older women found that in the older group, about 79% of eggs had abnormal spindle structures and misaligned chromosomes during the second meiotic division. In the younger group, only about 17% showed similar problems.

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The spindle is the molecular scaffold that physically pulls chromosomes apart during division. When it is malformed, chromosomes end up in the wrong cells. Compounding this problem, the quality-control system that normally catches such errors appears to be weaker in meiosis II than in meiosis I. Research has shown that the checkpoint meant to halt division when chromosomes are misaligned is relatively insensitive during the second meiotic division, meaning misaligned chromosomes get randomly distributed into the resulting cells rather than triggering a stop signal.

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This combination of deteriorating hardware and lax quality control explains the steep rise in chromosomal abnormalities in pregnancies of older mothers. It also explains why fertility treatments increasingly involve genetic screening of embryos before implantation: the goal is to identify which embryos made it through both meiotic divisions without picking up or losing chromosomes.

Genetic Variants That Disrupt Either Division

Beyond age-related wear, inherited genetic mutations can directly interfere with the meiotic machinery at specific stages. Some variants disrupt the processes of prophase I, when chromosomes pair up and recombine. Others affect the mechanisms that control when meiosis resumes after its long arrest, or how chromosomes are physically sorted during either division. These mutations are a recognized cause of female infertility, because eggs that cannot complete meiosis properly either never mature or produce embryos with lethal chromosomal errors.

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Identifying the specific gene involved can sometimes inform clinical decisions. If a woman’s infertility stems from a variant that blocks chromosome pairing during meiosis I, for example, the prognosis and treatment options differ from a case where the defect lies in the spindle machinery of meiosis II. Genetic testing for meiotic gene variants is still not routine in fertility clinics, but it is an area of active research.

Organisms That Flip the Order

For most organisms, meiosis I (the reductional division separating homologs) comes first, followed by meiosis II (the equational division separating sister chromatids). That sequence is so widespread that it was long assumed to be universal. It is not. Some organisms run the two divisions in reverse order, performing the equational split first and the reductional split second. This is called inverted meiosis.

Inverted meiosis has been documented in certain plants with an unusual chromosome structure called holocentric chromosomes, where the attachment point for the cell’s pulling machinery is spread along the entire chromosome rather than concentrated at a single centromere. In the sedge species Rhynchospora pubera and R. tenuis, researchers found that sister chromatids are pulled apart during the first division and homologous chromosomes are separated during the second, exactly the reverse of the standard sequence.

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Even more surprising, inverted meiosis doesn’t always require such exotic chromosome architecture. Research on organisms with conventional centromeres has shown that when a centromere changes its position on a chromosome, the affected chromosome can undergo meiosis in the inverted order while other chromosomes in the same cell proceed normally. This means both orders of division can happen simultaneously inside a single cell, revealing a flexibility in meiotic machinery that was not previously appreciated.

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Organisms That Skip Meiosis Entirely

If two divisions are the standard, some organisms have found creative workarounds that eliminate or heavily modify the process. In apomictic parthenogenesis, females produce offspring without fertilization by suppressing meiosis altogether and using mitosis-like cell divisions instead. The result is offspring that are genetic clones of the mother.

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Aphids take this a step further with cyclical parthenogenesis, alternating between sexual and asexual reproduction depending on environmental conditions. During their asexual generations, they modify meiosis during egg production, bypassing the normal cell-cycle checkpoints and producing eggs that develop without fertilization. When conditions shift (typically as winter approaches), they switch back to standard sexual reproduction with conventional meiosis.

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These variations underscore that the two-division structure of meiosis, while overwhelmingly common, is not the only way organisms solve the problem of reproduction. Natural selection has produced a spectrum of modifications, from subtle tweaks to the division order to outright elimination of the process.

How Meiosis Might Have Evolved

The two-division structure of meiosis is complex enough that it almost certainly did not appear all at once. One influential model proposes that meiosis evolved in a series of steps from simpler forms of cell division. The earliest ancestor of meiosis, according to this hypothesis, may have been a crude form of chromosome reduction achieved through a burst of faulty mitotic divisions (nondisjunctions) that happened to drop the chromosome number back down to a single set. Over evolutionary time, this sloppy process was refined into the precise two-division sequence we see today, with each refinement offering an immediate survival advantage.

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The addition of crossing over during prophase I would have been one of the most consequential evolutionary upgrades, because it introduced the ability to generate new combinations of genes within a single chromosome. Before crossing over, the only genetic shuffling came from the random sorting of whole chromosomes during the first division. With crossing over, even genes sitting on the same chromosome could be recombined. That additional diversity gave populations more raw material for natural selection to work with, which likely gave meiosis a strong evolutionary edge over simpler reproductive strategies. The two-division format was the scaffold that made all of this molecular shuffling possible.