Abstract
Sox5 belongs to the Sry-related HMG box gene family, which encodes transcription factors controlling cell fate and differentiation in many lineages. Sox5 produces a long L-Sox5 protein in neuronal, glial, neural crest, cartilage, and other cells, and a short Sox5 protein in spermatids. Sox5(-/-) mice have revealed essential roles for L-Sox5 in development but their neonatal death has prevented postnatal studies. We show here that we have generated mice harboring a conditional null allele for L-Sox5 (Sox5(fl+)) by flanking the fifth coding exon with loxP sites. Cre recombinase-mediated conversion of Sox5(fl+) into Sox5(fl-) abolishes L-Sox5 expression. Expectedly, Sox5(fl+/fl+) mice are indistinguishable from wildtype mice, and Sox5(fl-/fl-) mice from Sox5(-/-) mice. Moreover, the chondrodysplasia of Sox5(fl+/fl+)Sox6(fl+/fl+)Prx1Cre mice demonstrates that the two redundant chondrogenic Sox genes can be efficiently inactivated in a cell type-specific manner. This Sox5 conditional null allele will be valuable in further uncovering the in vivo roles of L-Sox5.