Breeds In Place
Because so many genetic and developmental components interact in pigmentation, it is not surprising that pigmentation defects show great interindividual and/or mutation-particular variability, even those derived from mutations in a single gene. For instance, the nicely-studied W and Steel mutations in mice (which contain the Kit/Steel Factor signaling pathway) can produce overall albinism, white recognizing, white toes, or a broad white “sash” depending on genetic background and the specific mutation (Jackson 1994). Nonetheless, there’s a clear tendency in each mouse mutants and domesticated species for pigmentation deficits to be more visible further from the site of origin of the neural crest, such as the paws or the midline of the stomach (Jackson 1994; Yamaguchi et al. 2007; Mills and Patterson 2009).
Such epistatic results, combined with the pleiotropy of most genes concerned in neural crest, imply that the consequences of neural crest discount are quite variable each between and inside species. We are conscious of no single mutation or scientific syndrome that may reproduce all and only the phenotypic effects of the DS but that is as expected, provided that we are not hypothesizing that the DS derives from changes in one or a few genes. Instead, the data above clearly assist the co-prevalence of multiple components of the DS as mixed effects of multiple NCC-affecting mutations and, when considered as a whole, all the elements are known to end result from NCC-associated genetic effects. Taken together with the experimental domestication information, these knowledge strongly help a … Read More