Goldfish are one of the most popular models for studying the genetic diversity of skin color. Thus, this study experimentally demonstrates that the rapid genetic fixation of morphological mutations during a short domestication time period may be related to the robustness of embryonic developmental mechanisms. Once this gene lost its original function in the twin-tail goldfish lineages, the dorsal-finless phenotype could be highly expressed. Based on these findings, we propose that chdSwt may have masked the expression of the dorsal-finless phenotype, acting as a capacitor buffering gene to allow accumulation of genetic mutations. Our F2 backcrossing and functional analyses revealed that the penetrance/expressivity of the dorsal-finless phenotype can be suppressed by the wild-type allele of chdS. Here, we demonstrate that the chordin gene, a key factor in dorsal-ventral patterning, is responsible not only for the twin-tail phenotype but also for the dorsal-finless phenotype. However, little is known about how these two different mutations could have co-occurred during such a short time period. These two mutated phenotypes appeared almost simultaneously within a short time frame (~600 years) and were fixed in several strains. Among them, the twin-tail and dorsal-finless phenotypes have particularly intrigued early and recent researchers, as equivalent morphologies are extremely rare in nature. Breeders and fanciers have established many peculiar morphological phenotypes in ornamental goldfish.
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