This article is from the WSSF 2008 AFRMA Rat & Mouse Tales news-magazine.
By Virginia Pochmann
From Mouse Review, Issue No. 4 (February 1989). Permission given to reprint article.
Occasionally a fancier will write and ask me if I can explain why his/her mouse with a new coat pattern never produced any offspring like itself. In most cases where the mutant animal does not reproduce itself, the reason is that it was a “somatic mutation.” This means that the mutation (change in the gene for coat color) occurred only in the body cells (“soma” means “body”) and did not extend to the all-important germ cells (egg or sperm) of that individual.
A somatic mutation is a change in a gene which happens to occur in a body cell during the development of the embryo. An example of this would be as follows: during embryonic development of a Self Black mouse, a mutation occurs in a body cell which changes the coat color to yellow in that cell. Now, all skin cells which are later descendants of that mutant cell will be carrying the gene for yellow, not for black, and will produce a patch of yellow hair on the otherwise Black mouse. This individual mouse now has some skin cells which are genetically Black and produce black hair, and some skin cells which are genetically yellow and produce yellow hair. This makes this mouse a “mosaic” mouse (an individual which has some parts of the body with one gene and some parts with another).
Physically it is a Black mouse with one or more patches of yellow hair, making it a bi- color mouse. If this mutation occurred on a white-spotted Black mouse, it would now be a tri-color mouse (black, white, and yellow). The Mouse Fancy has long awaited a strain of true-breeding Tri-color mice, and the fancier who finds such an individual in his/her colony is always hopeful that here at last is one which will breed true. So far, none of these ever have bred true because all of them have been somatic mutations, and none have had a mutant gene for patches of a different color carried into the gonads (ovaries or testes) where it could produce eggs or sperm which would perpetuate the pattern into the next generation.
Another example of a somatic mutation occurs frequently in the strain of mice known as “p-unstable” (pun). This gene, p-unstable, on a non-agouti mouse, produces pink-eyed grey mice just like those produced by the regular pink-eyed gene (p). These mice are the color known in the U.S.A. as Lilac, in England as Dove. The only difference from the regular p gene is that pun is unstable . . . meaning that it easily mutates back to the “P” state during embryonic development. If it does mutate, it produces grey mice with pink eyes which have one or more black patches in the coat. These bi-color mice are mosaics, their grey skin cells having the genotype of pun/pun, and their black skin cells having the genotype P/pun.
In p-unstable, the mosaic mice show mutant color patches which tend to begin or end at the top and bottom midlines of the mouse. This is because skin develops on the embryo beginning at the spine (dorsal midline) and grows downward over the sides of the mouse until it meets with the skin from the other side at the center of the belly (ventral midline). Thus, if the somatic mutation occurs early during skin development, the solid color patch will begin at or near the spine and grow downwards over the sides. If the mutation occurs somewhat later, the solid color patch may begin somewhat lower down on the side of the animal, and may or may not continue to the middle of the belly. Much variation is possible here, but often the animal will have an attractive checkerboard pattern of light and dark patches due to this pattern of skin growth on the embryo.
In the majority of individuals, no mutations will occur at the critical stage of development, and the entire animal will be all-over Lilac.
Ed. Note by Karen Robbins: Virginia thought that perhaps the Roan/Merle mice that showed up in Jack Ball’s colony in 1985 (in San Jose, CA), were perhaps a form of somatic mosaic. She got some of these Roans and did extensive breeding and testing and found them to be a recessive gene. She wrote an article “Explanation of Roan Mouse Inheritance Factors” that appeared in the S/O ’88 AFRMA Rat & Mouse Tales and is also in the AFRMA Mouse Genetics book. She sent some to the National Cancer Institute in 1988 to have the gene mapped out and determine which chromosome it was located on. Unfortunately, in a recent conversation with her she did not remember the results or the doctor doing the work.