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

13 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
Publication statusPublished - Dec 1 2007
Externally publishedYes



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

ASJC Scopus subject areas

  • Genetics
  • Endocrinology
  • Cell Biology

Cite this

Walker, W. P., Aradhya, S., Hu, C. L., Shen, S., Zhang, W., Azarani, A., ... Gunn, T. M. (2007). Genetic analysis of attractin homologs. Genesis, 45(12), 744-756.