What Occurs in Meiosis: Two Divisions Explained

Meiosis is a type of cell division that cuts a cell’s chromosome count in half, turning one cell with 46 chromosomes into four cells with 23 chromosomes each. It accomplishes this through two back-to-back rounds of division, called meiosis I and meiosis II, that follow a single round of DNA replication. The process produces sperm and egg cells (gametes) and is the reason offspring aren’t genetic clones of their parents.

DNA Replication Happens Once, Division Happens Twice

Before meiosis begins, the cell copies all of its DNA. Each chromosome becomes a pair of identical sister chromatids joined at a point called the centromere. A human germ cell starts with 46 chromosomes, and after replication it still has 46 chromosomes, but each one is now a double structure made of two identical halves.

The cell then divides twice without copying its DNA again. This is the key to halving the chromosome number. The first division separates matched pairs of chromosomes (one from your mother, one from your father). The second division splits the sister chromatids apart. The result: four cells, each with 23 single chromosomes.

Meiosis I: Separating Paired Chromosomes

The first division is where meiosis looks most different from ordinary cell division. Its defining feature is that homologous chromosomes, the maternal and paternal versions of each chromosome, pair up and then move to opposite ends of the cell.

Prophase I and Crossing Over

Prophase I is the longest and most complex phase. It’s traditionally broken into five sub-stages (leptotene, zygotene, pachytene, diplotene, and diakinesis), though what matters most is what they accomplish together. During this phase, each pair of homologous chromosomes finds its partner and lines up side by side. A protein structure called the synaptonemal complex forms between them, working like a zipper to hold the pair tightly together along their full length. The paired chromosomes, now called a bivalent, look like a four-stranded bundle because each chromosome is already made of two sister chromatids.

While the chromosomes are zipped together, something remarkable happens: crossing over. The DNA in a maternal chromatid and a paternal chromatid physically breaks, and the broken ends swap between the two. This exchange, called genetic recombination, shuffles alleles between the mother’s and father’s chromosomes. The points where the swap occurred become visible as X-shaped structures called chiasmata once the synaptonemal complex disassembles. Crossing over means the chromosomes that come out of meiosis are not identical to the ones that went in.

Metaphase I Through Telophase I

After prophase I, the paired chromosomes line up along the middle of the cell during metaphase I. Each bivalent orients randomly, so the maternal chromosome might face one pole and the paternal chromosome the other, or vice versa. This random arrangement is called independent assortment, and it’s a second major source of genetic variation. In humans, with 23 pairs of chromosomes, independent assortment alone can produce roughly 8 million different combinations of maternal and paternal chromosomes in each gamete.

During anaphase I, the homologous chromosomes are pulled to opposite poles. Critically, the sister chromatids stay together. Each side of the cell now has 23 chromosomes, each still made of two joined chromatids. The cell divides in telophase I, producing two daughter cells that are haploid in chromosome number but still have double-structured chromosomes.

Meiosis II: Splitting Sister Chromatids

Between the two divisions there is a brief interphase, sometimes called interkinesis. No DNA replication occurs during this gap. The two daughter cells from meiosis I move straight into a second round of division that closely resembles ordinary cell division (mitosis).

In meiosis II, the 23 chromosomes in each cell line up individually at the cell’s center during metaphase II. During anaphase II, the sister chromatids finally separate and are pulled to opposite poles. Each cell divides again, so the two cells from meiosis I become four. Each of the four resulting cells contains 23 single chromosomes, one complete set of genetic instructions.

How Meiosis Differs in Males and Females

In males, meiosis doesn’t begin until puberty, when spermatogenesis starts. Each round of meiosis produces four functional sperm cells, and the process continues throughout life. In females, germ cells enter meiosis during fetal development, pausing partway through prophase I. Meiosis resumes at puberty, one egg at a time, with each menstrual cycle. Rather than producing four equal cells, female meiosis generates one large egg and smaller nonfunctional cells called polar bodies, concentrating the cytoplasm and nutrients into a single gamete.

This difference in timing has practical consequences. Because female germ cells are arrested in meiosis I for years or even decades, the machinery holding chromosomes together has more time to degrade, which increases the chance of errors in older eggs.

Two Engines of Genetic Diversity

Meiosis generates genetic variation through two primary mechanisms that work together. Crossing over during prophase I physically recombines DNA between maternal and paternal chromosomes, creating chromatids with new combinations of alleles that didn’t exist on either parent chromosome. Independent assortment during metaphase I randomizes which version of each chromosome ends up in each gamete. Combined, these two processes ensure that every sperm or egg cell is genetically unique.

This reshuffling is thought to be the fundamental advantage of sexual reproduction. By reducing genetic associations between different gene locations and creating new allele combinations each generation, meiosis gives populations the raw material to adapt to changing environments. One evolutionary hypothesis suggests that the elaborate pairing and recombination machinery originally evolved to repair DNA damage, then was co-opted for generating diversity.

What Happens When Meiosis Goes Wrong

The most common meiotic error is nondisjunction, where chromosomes fail to separate properly. When this happens during anaphase I, the homologous chromosomes both get pulled to the same side. The result is two daughter cells with an extra chromosome (designated n+1) and two with a missing one (n-1). All four gametes from that cell are abnormal.

Nondisjunction can also occur during meiosis II, when sister chromatids fail to split apart. This is slightly less damaging in scope: two of the four resulting cells will have normal chromosome counts, while the other two will be n+1 and n-1. If an abnormal gamete is fertilized, the resulting embryo ends up with too many or too few chromosomes, a condition called aneuploidy.

Several well-known genetic conditions result from nondisjunction:

  • Down syndrome: three copies of chromosome 21 (trisomy 21)
  • Edwards syndrome: trisomy of chromosome 18
  • Patau syndrome: trisomy of chromosome 13
  • Turner syndrome: a female with only one X chromosome (45 total)
  • Klinefelter syndrome: a male with an extra X chromosome (47, XXY)

Most other trisomies and monosomies are so disruptive that they cause miscarriage early in development. The conditions listed above are among the few compatible with survival to birth, which is why they are the ones most commonly diagnosed.