| First Author | Walker WP | Year | 2007 |
| Journal | Genesis | Volume | 45 |
| Issue | 12 | Pages | 744-56 |
| PubMed ID | 18064672 | Mgi Jnum | J:130463 |
| Mgi Id | MGI:3771742 | Doi | 10.1002/dvg.20351 |
| Citation | Walker WP, et al. (2007) Genetic analysis of attractin homologs. Genesis 45(12):744-56 |
| abstractText | 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 beta-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. |
