Genetic analysis of attractin homologs

Will P. Walker, Swaroop Aradhya, Che Lin Hu, Shiliang Shen, Wei Zhang, Arezou Azarani, Xin Yun Lu, Gregory S. Barsh, Teresa M. Gunn

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Attractin (ATRN) and Attractin-like 1 (ATRNL1) are highly similar type I transmembrane proteins. Atrn null mutant mice have a pleiotropic phenotype including dark fur, juvenile-onset spongiform neurodegeneration, hypomyelination, tremor, and reduced body weight and adiposity, implicating ATRN in numerous biological processes. Bioinformatic analysis indicated that Atrn and Atrnl1 arose from a common ancestral gene early in vertebrate evolution. To investigate the genetics of the ATRN system and explore potential redundancy between Atrn and Atrnl1, we generated and characterized Atrnl1 loss- and gain-of-function mutations in mice. Atrnl1 mutant mice were grossly normal with no alterations of pigmentation, central nervous system pathology or body weight. Atrn null mutant mice carrying a β-actin promoter-driven Atrnl1 transgene had normal, agouti-banded hairs and significantly delayed onset of spongiform neurodegeneration, indicating that over-expression of ATRNL1 compensates for loss of ATRN. Thus, the two genes are redundant from the perspective of gain-of-function but not loss-of-function mutations.

Original languageEnglish (US)
Pages (from-to)744-756
Number of pages13
JournalGenesis
Volume45
Issue number12
DOIs
StatePublished - Dec 2007
Externally publishedYes

Keywords

  • Attractin
  • Attractin-like 1
  • Melanocortin signaling
  • Pigment type-switching
  • Spongiform neurodegeneration

ASJC Scopus subject areas

  • Genetics
  • Endocrinology
  • Cell Biology

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  • Cite this

    Walker, W. P., Aradhya, S., Hu, C. L., Shen, S., Zhang, W., Azarani, A., Lu, X. Y., Barsh, G. S., & Gunn, T. M. (2007). Genetic analysis of attractin homologs. Genesis, 45(12), 744-756. https://doi.org/10.1002/dvg.20351