It has been hypothesized that this is the result of a combination of mitotic recombination and natural selection within the skin.

These mutants are most likely defective in both the spontaneous and induced mitotic recombination processes.

One basic mechanism which can produce mosaic tissue is mitotic recombination or somatic crossing-over.

Mitotic recombination takes place during interphase.

Also mitotic recombination becomes deficient, mutation frequency increases and meiosis fails to complete.

The mechanisms behind mitotic recombination are similar to those behind meiotic recombination.

In addition, non-homologous mitotic recombination is a possibility and can often be attributed to non-homologous end joining.

Additionally, mitotic recombination can result in the expression of recessive genes in an otherwise heterozygous individual.

The discovery of mitotic recombination came from the observation of twin spotting in Drosophila melanogaster.

Later experiments uncovered when mitotic recombination occurs in the cell cycle and the mechanisms behind recombination.

Genetic mosaics are a particularly powerful tool when used in the commonly studied fruit fly, where they are created through mitotic recombination.

Mitotic recombination can happen at any locus but is observable in individuals that are heterozygous at a given locus.

More recently it was argued that the DNA break leading to mitotic recombination happened during G1, but repair happens after replication.

Mitotic recombination is a type of genetic recombination that may occur in somatic cells during mitosis in both sexual and asexual organisms.

In asexual organisms, the study of mitotic recombination is one way to understand genetic linkage because it is the only source of recombination within an individual.

In revertant mosaicism, the healthy tissue formed by mitotic recombination can outcompete the original, surrounding mutant cells in tissues like blood and epithelia that regenerate often.

This mutation leads to high rates of mitotic recombination in mice, and this recombination rate is in turn responsible for causing tumor susceptibility in those mice.

For use in experimentation with genomes in model organisms such as Drosophila melanogaster, mitotic recombination can be induced via X-ray and the FLP-FRT recombination system.

This twin spotting, or mosaic spotting, was observed in D. melanogaster as early as 1925, but it was only in 1936 that Curt Stern explained it as a result of mitotic recombination.

At the same time, mitotic recombination be beneficial: it may play an important role in repairing double stranded breaks, and it may be beneficial to the organism if having homozygous dominant alleles is more functional than the heterozygous state.

In cancer cells "global hypomethylation" due to disruption in DNA methyltransferases (DNMTs) may promote mitotic recombination and chromosome rearrangement, ultimately resulting in aneuploidy when the chromosomes fail to separate properly during mitosis.

Instead of using GFP to mark the wild type chromosome as above, GAL80 serves this purpose, so that when it is removed by mitotic recombination, GAL4 is allowed to function, and GFP turns on.

Cytogenetic studies localized the region to the long arm of chromosome 13, and molecular genetic studies demonstrated that tumorigenesis was associated with chromosomal mechanisms, such as mitotic recombination or non-disjunction, that could lead to homozygosity of the mutation.