Identification of Mutant Genes and Introgressed Tiger Salamander DNA in the Laboratory Axolotl, Ambystoma mexicanum View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-01-31

AUTHORS

M. Ryan Woodcock, Jennifer Vaughn-Wolfe, Alexandra Elias, D. Kevin Kump, Katharina Denise Kendall, Nataliya Timoshevskaya, Vladimir Timoshevskiy, Dustin W. Perry, Jeramiah J. Smith, Jessica E. Spiewak, David M. Parichy, S. Randal Voss

ABSTRACT

The molecular genetic toolkit of the Mexican axolotl, a classic model organism, has matured to the point where it is now possible to identify genes for mutant phenotypes. We used a positional cloning–candidate gene approach to identify molecular bases for two historic axolotl pigment phenotypes: white and albino. White (d/d) mutants have defects in pigment cell morphogenesis and differentiation, whereas albino (a/a) mutants lack melanin. We identified in white mutants a transcriptional defect in endothelin 3 (edn3), encoding a peptide factor that promotes pigment cell migration and differentiation in other vertebrates. Transgenic restoration of Edn3 expression rescued the homozygous white mutant phenotype. We mapped the albino locus to tyrosinase (tyr) and identified polymorphisms shared between the albino allele (tyra) and tyr alleles in a Minnesota population of tiger salamanders from which the albino trait was introgressed. tyra has a 142 bp deletion and similar engineered alleles recapitulated the albino phenotype. Finally, we show that historical introgression of tyra significantly altered genomic composition of the laboratory axolotl, yielding a distinct, hybrid strain of ambystomatid salamander. Our results demonstrate the feasibility of identifying genes for traits in the laboratory Mexican axolotl. More... »

PAGES

6

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-017-00059-1

DOI

http://dx.doi.org/10.1038/s41598-017-00059-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1079403228

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28127056


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