What Type of Cells Undergo Meiosis?

Only germ cells, the dedicated reproductive cells of an organism, undergo meiosis. In animals, that means the precursor cells of sperm and eggs inside the testes and ovaries. In plants, specialized cells called spore mother cells do the job. Even single-celled organisms like yeast and certain protists carry out meiosis, but only under specific conditions and only in cells that have the right chromosome count to begin with. The rest of the body’s cells, the somatic cells that make up skin, muscle, brain, and everything else, divide exclusively by mitosis and never enter a meiotic program.

Germ Cells Get Their Identity Early

Before any cell can undergo meiosis, it first has to be designated as a germ cell. In many animals, that designation happens remarkably early in embryonic development. Primordial germ cells, often abbreviated PGCs, are specified during early embryogenesis, and their development initiates the lineage that will eventually pass genetic information from one generation to the next.¹ In some species, germ-line determinants are packaged into certain cells before the rest of the embryo’s cell types are even established. Not every animal follows the same playbook, though. In axolotls, for example, PGCs are maintained by signals from surrounding cells, and germ-line commitment happens later, after the embryo has already completed gastrulation.²

In humans, the molecular details of PGC specification have been studied using stem cells grown in the lab. SOX17, a transcription factor, turns out to be a key driver of human germ-cell fate, while another protein called BLIMP1 works to shut down genes that would push cells toward becoming gut tissue or other body parts instead.³ Once a cell is locked into the germ-line path, it migrates to the developing gonad, where it will eventually receive the signals to begin meiosis. Without that journey and those signals, meiosis simply does not start.

Spermatocytes in Males

In the testes, germ cells called spermatogonia sit along the outer edge of the seminiferous tubules and divide by mitosis to keep the supply of precursors going. When one of these cells commits to producing sperm, it becomes a primary spermatocyte, the cell that actually enters meiosis I.⁴ After the first meiotic division, the resulting secondary spermatocytes quickly proceed through meiosis II, producing four haploid spermatids that then mature into functional sperm.

This process is continuous from puberty onward. A man in his twenties and a man in his sixties are both producing new spermatocytes and completing meiosis, though sperm quality tends to decline with age. The entire trip from spermatogonium to mature sperm takes roughly two to three months in humans, and the testes churn out millions of sperm per day. Meiosis in males is symmetrical: one primary spermatocyte ultimately yields four functional sperm cells, each carrying half the original chromosome number.

Oocytes in Females

The female side of the story is strikingly different. In human females, PGCs transition from mitotic division to meiotic entry during fetal development. Germ cells in the fetal ovary begin meiosis and then stall. They arrest at a specific point in the first meiotic division, the diplotene stage of prophase I, after homologous chromosomes have paired up and swapped segments of DNA but before they physically separate.⁵ This arrest is maintained by high levels of a signaling molecule called cyclic AMP inside the oocyte.

An oocyte can sit in this arrested state for years or even decades. A girl is born with her oocytes already paused partway through meiosis I. Only after puberty, when a surge of luteinizing hormone triggers ovulation each month, does one oocyte (or occasionally more) resume meiosis.⁶ Even then, the oocyte only completes meiosis I at ovulation and pauses again at metaphase of meiosis II. It finishes the second division only if a sperm fertilizes it. Unlike the four equal cells produced in male meiosis, female meiosis is asymmetric: each division shunts most of the cytoplasm into the one functional egg cell while producing tiny, disposable polar bodies on the side.

Why Retinoic Acid Is the Starting Pistol

A question that puzzled researchers for a long time was what tells a germ cell to stop dividing by mitosis and start meiosis. A growing body of evidence points to retinoic acid, a derivative of vitamin A, as the key signal in both males and females.⁷ In mouse studies, researchers showed that retinoic acid levels are higher in the fetal ovary than in the fetal testis at the stage when female germ cells are entering meiosis. Adding retinoic acid to cultured fetal testis tissue was enough to push male germ cells into meiotic prophase prematurely, and blocking retinoic acid signaling in fetal ovary tissue prevented female germ cells from entering meiosis at all.⁸

Retinoic acid works in part by switching on a gene called STRA8, which encodes a protein needed for the pre-meiotic DNA replication step. In female mouse germ cells, STRA8 interacts with a cell-cycle regulator called RB to help the cell transition into the S phase of meiosis and activate meiotic genes. When researchers mutated the site where STRA8 binds RB, meiotic entry was delayed, and the resulting mice lost oocytes prematurely.⁹ In males, the testes actively break down retinoic acid during fetal life using an enzyme called CYP26B1, which is why male germ cells don’t start meiosis until after birth. The timing is all about controlling when and where retinoic acid is available.

Meiosis in Plants

Plants don’t have testes or ovaries, but they absolutely rely on meiosis for sexual reproduction. The cells that undergo meiosis in flowering plants are called spore mother cells. In the ovule, a diploid megaspore mother cell undergoes meiosis to produce megaspores, which develop into the female gametophyte (containing the egg cell).¹⁰ In the anthers (the pollen-producing structures), diploid microspore mother cells, also called microsporocytes, undergo meiosis to produce microspores that develop into pollen grains.

In broad beans, for instance, meiosis begins in microsporocytes before it starts in megaspore mother cells, showing that the timing of meiosis can differ between male and female reproductive structures even in the same plant.¹¹ The key difference from animals is the alternation of generations: the haploid products of meiosis don’t become sperm or eggs directly. Instead, they develop into a small multicellular gametophyte stage that then produces the sex cells by mitosis. But the meiotic step itself is still confined to these specific spore mother cells. Leaf cells, root cells, and stem cells never undergo meiosis.

Yeast and Protists

Single-celled organisms show that meiosis is not limited to complex multicellular life. In the budding yeast Saccharomyces cerevisiae, diploid cells undergo meiosis and produce haploid spores when starved of nitrogen and given a poor carbon source.¹² Sporulation is a stress response: when food runs out, the cell uses meiosis as a survival strategy, packaging the resulting haploid nuclei into tough spore coats.¹³ Only diploid yeast cells can enter meiosis. Haploid yeast cells must first mate with a cell of the opposite mating type to become diploid before they have the option.

Across the broader tree of eukaryotic life, conventional meiosis shows up in all major groups, including early-branching protists. Phylogenomic studies have found meiosis-specific genes in organisms as diverse as Giardia, Plasmodium (the malaria parasite), and kinetoplastids, arguing that meiosis was present in the common ancestor of all eukaryotes.¹⁴ Even species not previously known to undergo meiosis, like Entamoeba, carry some of the same meiosis-specific genes, hinting at undiscovered sexual cycles.¹⁵ In some protists classified as Rhizaria, researchers have detected expression of meiosis-associated genes during starvation-induced cell fusion, suggesting that even poorly studied organisms may be running some form of meiosis when conditions demand it.¹⁶

When Aging Oocytes Get Meiosis Wrong

One of the most medically significant consequences of meiosis happens in aging human eggs. Because oocytes arrest in prophase I before birth and don’t complete meiosis until decades later, the molecular machinery holding chromosomes together degrades over time. The protein complexes called cohesins, which keep paired chromosomes tightly bound, gradually weaken. This deterioration is now recognized as a leading cause of age-related aneuploidy, where eggs end up with the wrong number of chromosomes.¹⁷

Recent research has added another layer to this picture. A study of human oocytes found that age-dependent loss of a protective protein called SGO2 further weakens the already vulnerable cohesin at the centromere, the region of the chromosome that is most critical for ensuring the two copies separate properly.¹⁸ The result is a steady increase in chromosome segregation errors with maternal age. This is the biological basis for the well-known rise in conditions like Down syndrome in pregnancies of older mothers. The cells undergoing meiosis are doing so correctly in terms of identity; the problem is that the hardware they need to do it properly has been sitting on the shelf too long.

Meiosis in Polyploid Organisms

Most textbook descriptions of meiosis assume a neat, diploid organism with two copies of each chromosome. But many real-world species, especially plants, are polyploid: they carry three, four, six, or even more copies. Wheat, for example, is hexaploid (six sets). In newly formed polyploids, meiosis faces a logistical challenge because related chromosomes can pair up in complicated structures called multivalents, where three or more chromosomes attempt to synapse and recombine at the same time.¹⁹ Multivalent formation tends to cause missegregation and reduced fertility. Over time, many polyploid species evolve mechanisms to restrict pairing to true homologs, smoothing meiosis back toward the tidy two-by-two pattern.

Automixis and Restitutional Meiosis

Some organisms have found ways to use meiosis without traditional sex. In automixis, a form of parthenogenesis, meiosis proceeds but the haploid products fuse back together to restore the full chromosome number, producing offspring without fertilization by a mate.²⁰ The stick insects of the genus Bacillus illustrate just how varied these mechanisms can be. In one species, Bacillus atticus, nuclei from the first meiotic division fuse to restore diploidy, while in the related Bacillus rossius, diploidization happens later through a different restitution mechanism during early embryonic development.²¹

Restitutional meiosis takes a different shortcut. Instead of completing both divisions, the cell skips one. First division restitution skips meiosis I entirely, converting the process into something resembling a mitotic division and producing gametes that retain the full parental chromosome number along with most or all of the parent’s genetic diversity. Second division restitution skips meiosis II instead, preserving the crossover events of meiosis I but still producing unreduced gametes that keep roughly a third to two-fifths of the parent’s heterozygosity.²² These unreduced gametes are a major route by which new polyploid species arise in plants.

Parasexual Cycles Without True Meiosis

Not every chromosome-number reduction involves actual meiosis. The human fungal pathogen Candida albicans is a striking example. In its parasexual cycle, diploid cells mate to form tetraploid cells, which then return to roughly the diploid state through a non-meiotic process of concerted chromosome loss rather than through orderly meiotic divisions.²² This chromosome loss is somewhat random, frequently producing aneuploid cells with uneven chromosome numbers. Researchers have described a related process they call “parameiosis,” in which Candida tetraploid cells undergo a form of depolyploidization that involves homologous recombination but still falls short of true meiosis.²³

The parasexual cycle generates genetic diversity through recombination and chromosome reassortment without the full meiotic apparatus. It illustrates that while meiosis is the standard mechanism for halving chromosome numbers across eukaryotes, organisms can cobble together alternative reductional strategies. These alternatives blur the boundary between “meiotic” and “non-meiotic,” and they remind us that the question of which cells undergo meiosis sometimes has a less clean answer than textbooks suggest.

Making Germ Cells in the Lab

One of the more ambitious frontiers in reproductive biology involves coaxing stem cells to undergo meiosis outside the body. Researchers have successfully induced human pluripotent stem cells to become primordial germ cells and then pushed those lab-made PGCs to resume meiosis and differentiate into primary oocytes. In one approach, activating the Wnt signaling pathway was enough to restart meiosis in dormant induced PGCs and move them toward oocyte-like cells.²⁴ The cells still needed a supporting niche of ovarian-like tissue to proceed, reflecting the fact that mammalian germ cells only undergo meiosis in the context of the gonad, surrounded by somatic support cells that regulate the pace and timing of the process.

These experiments are still far from producing viable human eggs for fertility treatment, but they have opened windows into the basic requirements for meiosis. They confirm that the cell’s identity as a germ cell is necessary but not sufficient; the right signaling environment must also be in place. For people facing infertility due to premature loss of germ cells or gonadal dysfunction, this line of research holds long-term promise, though clinical applications remain years away.

When Somatic Cells Borrow Meiotic Genes

Under normal circumstances, somatic cells never undergo meiosis. But cancer, as it so often does, breaks the rules. In certain tumors, particularly those with mutations in the tumor suppressor p53, researchers have observed aberrant expression of proteins normally restricted to meiosis. Polyploid giant cancer cells, which arise when tumor cells fail to divide properly and accumulate extra chromosome sets, sometimes appear to use meiotic-like machinery during a process called depolyploidization, where they shed excess chromosomes and return to a more typical chromosome number. This process shares features with meiotic prophase, though it is disorganized and error-prone compared with genuine meiosis in germ cells. The expression of meiotic proteins in these cancer cells is abnormal, not a sign that somatic cells have secretly gained the ability to undergo real meiosis. Instead, it reflects the chaotic gene regulation of aggressive tumors co-opting whatever molecular tools happen to be available.