The diatom life cycle

A key feature of the diatoms’ haplo-diploid life cycle is a unique strategy to switch between the reduction of cell size during somatic divisions and its restitution during sexual reproduction. Asexually propagating diploid diatom cells divide mitotically, becoming smaller with each division due to the mechanics of their cell wall formation. Diatom cell walls, called frustules, have two valves that typically overlap one another – the bigger top valve called the epitheca and the smaller bottom valve called the hypotheca. After a mitotic division, each of the two daughter cells inherits one of the valves that serve as an epitheca, and forms a new hypotheca during the cell cycle. As a result, the average size of a proliferating diatom population decreases with each division cycle. The restoration of cell size occurs through sexual reproduction. Vegetative cells undergo meiosis and produce gametes that fuse to form a zygote. The zygote grows into a large sphere covered by an organic membrane, the auxospore. A new large cell, the initial, is formed inside the auxospore envelope, which then begins a new round of vegetative multiplication after restoration of the silica exoskeleton. The induction of sex is strictly size-dependent: only cells of a particular size range - small cells, below the sexual size threshold - are able to initiate meiosis. Cells that fail to reproduce sexually will continue to divide mitotically until they reach a critical minimal size, at which point they die. The specific modes of sexual reproduction differ between the two major diatom groups, the centrics and the pennates. Centrics are mostly homothallic and one clone is capable of forming large egg cells as well as motile, flagellated sperm cells. In contrast, pennate diatoms are mostly heterothallic, and sexual reproduction is initiated by cell-cell interactions between vegetative cells from different sexually compatible clones, requiring the production of multiple pheromones. In both pennate and centric diatoms, auxosporulation is secondarily and species-specifically influenced by external factors such as irradiance, day length and temperature. 

Genetic variability is essential for the long-term survival of species, but individual organisms must also preserve their genetic integrity. Eukaryotes have evolved two distinct modes of cell division, meiosis and mitosis, to balance these opposing needs.

Meiosis generates haploid gametes and promotes genetic diversity by recombining homologous chromosomes during prophase I. This process, known as interhomolog homologous recombination (IH-HR), is part of a specialised cellular program that creates novel allelic combinations, ensures proper chromosome pairing and segregation, and ultimately transmits genetic diversity to the next generation.

Mitosis, in contrast, serves to faithfully replicate a cell’s genome, producing two genetically identical daughter cells. During the mitotic cycle, especially after DNA replication, homologous recombination (HR) is one of the main DNA repair pathways used to repair DNA double-strand breaks (DSBs), a dangerous form of DNA damage. However, in contrast to meiosis, vegetative cells strongly favour using the sister chromatid as the repair template. This preference ensures error-free repair due to the sequence identity between sister chromatids, maintaining genomic stability.

Recombination between homologous chromosomes during mitosis, is largely avoided because it can be harmful. Unlike sister chromatids, homologous chromosomes often contain sequence differences, so IH-HR can result in unwanted genetic changes such as loss of heterozygosity (LOH), copy number variation (CNV), or chromosomal rearrangements. These changes are particularly dangerous in multicellular organisms, where they can accumulate and contribute to cancer development.

Because of these risks, most eukaryotic cells have evolved mechanisms to suppress IH-HR during mitosis. The sister chromatid is kept in close proximity through cohesion and nuclear architecture, making it the preferred repair template. In contrast, meiotic cells express specific proteins that promote homolog recognition and pairing, overriding this bias to enable recombination between homologs.

While this system safeguards genome integrity, it also limits the ability to introduce controlled genetic variation. In biotechnology and agriculture, for example, generating new allelic combinations often relies on rare and unevenly distributed meiotic crossovers. Understanding—and potentially harnessing—IH-HR in mitotic cells could therefore have far-reaching implications, both for basic biology and applied research.