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 journalArticlepeer-review

16 Scopus citations


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
Issue number12
StatePublished - Dec 2007
Externally publishedYes


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

ASJC Scopus subject areas

  • Genetics
  • Endocrinology
  • Cell Biology


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