Fktn (fukutin) is one of several genes that are required for dystoglycan processing. Deficiencies in dystroglycan are associated with an array of congenital and limb girdle muscular dystrophies (dystroglycanopathies). 

These mice carry a floxed allele of Fktn. Homozygotes are born at reduced Mendelian frequencies and have reduced fertility. Viable animals have an overtly normal phenotype. Dystroglycan is properly glycosylated in all tissues tested. 

When crossed with a Cre strain, tissue-specific or inducible knockouts of the gene can be generated. Crosses with Myf5 (myogenic factor 5) (Stock No. <a href="https://www.jax.org/strain/007893">007893</a>) and Ckm (creatine kinase, muscle) (Stock No. <a href="https://www.jax.org/strain/006405">006405</a>) Cre strains generate dystroglycanopathy mice representative of a spectrum of mild to severe patient diseases. Conditional disruption during muscle development at E8 causes a more severe phenotype than knockouts initiated at E17. A corresponding deficiency of functionally glycosylated dystroglycan along with dystrophic histopathology supports a role for dystroglycan in muscle development or differentiation.

These mice carry a floxed allele of Fktn (fukutin). When crossed with a Cre strain, tissue-specific knockouts of the gene can be generated. Crosses with Myf5 (myogenic factor 5) and Ckm (creatine kinase, muscle) Cre strains generate dystroglycanopathy mice representative of a spectrum of mild to severe patient diseases.

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