These Ift88fl mice possess loxP sites flanking exons 4-6 of the intraflagellar transport 88 (Ift88) gene. IFT maintain primary cilia that are present on most cell types, and mediates bidirectional movement of structural and signaling components during events such as development and wound healing. Mutations in cilia-related genes, such as Itf88, have been implicated in many ciliopathic human genetic diseases. Mice that are homozygous for this allele are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 4-6 deleted in cre-expressing tissues.
For example, when crossed to B6.Cg-Tg(Prrx1-cre)1Cjt/J mice (Stock No. 005584) expressing Cre recombinase in early limb bud mesenchyme, resulting offspring exhibit extensive polydactyly with loss of anteroposterior digit patterning and shortening of the proximodistal axis.
When crossed to B6;SJL-Tg(Col2a1-cre)1Bhr/J (Stock No. 003554) expressing Cre recombinase in differentiating chondrocytes, notochord and submandibular glands, resulting offspring exhibit depletion of chrondocyte cilia, premature loss of the growth plate and post-natal dwarfism.
