IFT27, encoding a small GTPase component of IFT particles, is mutated in a consanguineous family with Bardet-Biedl syndrome

Mohammed A. Aldahmesh, Yuanyuan Li, Amal Alhashem(Riyadh Armed Forces Hospital), Shams Anazi, H. Alkuraya(Imam Mohammad ibn Saud Islamic University), M. Hashem, Ali Awaji(King Fahad Central Hospital), Samira Sogaty(King Fahad Hospital Jeddah), Abdullah S. Al-Kharashi(King Saud University), S. Alzahrani(Riyadh Armed Forces Hospital), S. A. Al Hazzaa(Alfaisal University), Yong Xiong(Yale University), Seong-Ho Kong, Zhaoxia Sun(Fujikura (United States)), Fowzan S. Alkuraya(Alfaisal University)
Human Molecular Genetics
January 31, 2014
Cited by 141Open Access
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Abstract

Bardet-Biedl syndrome (BBS) is an autosomal recessive ciliopathy with multisystem involvement. So far, 18 BBS genes have been identified and the majority of them are essential for the function of BBSome, a protein complex involved in transporting membrane proteins into and from cilia. Yet defects in the identified genes cannot account for all the BBS cases. The genetic heterogeneity of this disease poses significant challenge to the identification of additional BBS genes. In this study, we coupled human genetics with functional validation in zebrafish and identified IFT27 as a novel BBS gene (BBS19). This is the first time an intraflagellar transport (IFT) gene is implicated in the pathogenesis of BBS, highlighting the genetic complexity of this disease.


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