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Background  Mice homozygous for the juvenile alopecia mutation ( jal ) display patches of hair loss that appear as soon as hair develops in the neonatal period and persist throughout life. Although a report initially describing this mouse variant suggested that  jal  maps to mouse Chromosome 13, our preliminary mapping analysis did not support that claim.    Results  To map  jal  to a particular mouse chromosome, we produced a 103-member intraspecific backcross panel that segregated for  jal,  and typed it for 93 PCR-scorable, microsatellite markers that are located throughout the mouse genome. Only markers from the centromeric tip of Chromosome 2 failed to segregate independently from  jal , suggesting that  jal  resides in that region. To more precisely define  jal ’s location, we characterized a second, 374-member backcross panel for the inheritance of five microsatellite markers from proximal Chromosome 2. This analysis restricted  jal ’s position between  D2Mit359  and  D2Mit80 , an interval that includes  Il2ra  (for interleukin 2 receptor, alpha chain), a gene that is known to be associated with alopecia areata in humans. Complementation testing with an engineered null allele of  Il2ra , however, showed that  jal  is a mutation in a distinct gene. To further refine the location of  jal , the 374-member panel was typed for a set of four single-nucleotide markers located between  D2Mit359  and  D2Mit80 , identifying a 0.55 Mb interval where  jal  must lie. This span includes ten genes—only one of which,  Gata3  (for GATA binding protein 3)—is known to be expressed in skin. Complementation testing between  jal  and a  Gata3  null allele produced doubly heterozygous, phenotypically mutant offspring.    Conclusions  The results presented indicate that the  jal  mutation is a mutant allele of the  Gata3  gene on mouse Chromosome 2. We therefore recommend that the  jal  designation be changed to  Gata3   jal   ,  and suggest that this mouse variant may provide an animal model for at least some forms of focal alopecia that have their primary defect in the hair follicle and lack an inflammatory component.

The juvenile alopecia mutation (jal) maps to mouse Chromosome 2, and is an allele of GATA binding protein 3 (Gata3)