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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 (Sox5fl+) by flanking the fifth coding exon with loxP sites. Cre recombinase‐mediated conversion of Sox5fl+ into Sox5fl− abolishes L‐Sox5 expression. Expectedly, Sox5fl+/fl+ mice are indistinguishable from wildtype mice, and Sox5fl−/fl− mice from Sox5−/− mice. Moreover, the chondrodysplasia of Sox5fl+/fl+Sox6fl+/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. genesis 46:294–299, 2008.
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Dy et al. (2008) studied this question.
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