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BBS mutations modify phenotypic expression of CEP290-related ciliopathies
Journal article   Open access   Peer reviewed

BBS mutations modify phenotypic expression of CEP290-related ciliopathies

Yan Zhang, Seongjin Seo, Sajag Bhattarai, Kevin Bugge, Charles C Searby, Qihong Zhang, Arlene V Drack, Edwin M Stone and Val C Sheffield
Human molecular genetics, Vol.23(1), pp.40-51
01/01/2014
DOI: 10.1093/hmg/ddt394
PMCID: PMC3857943
PMID: 23943788
url
https://doi.org/10.1093/hmg/ddt394View
Published (Version of record) Open Access

Abstract

Ciliopathies are a group of heterogeneous disorders associated with ciliary dysfunction. Diseases in this group display considerable phenotypic variation within individual syndromes and overlapping phenotypes among clinically distinct disorders. Particularly, mutations in CEP290 cause phenotypically diverse ciliopathies ranging from isolated retinal degeneration, nephronophthisis and Joubert syndrome, to the neonatal lethal Meckel-Gruber syndrome. However, the underlying mechanisms of the variable expressivity in ciliopathies are not well understood. Here, we show that components of the BBSome, a protein complex composed of seven Bardet-Biedl syndrome (BBS) proteins, physically and genetically interact with CEP290 and modulate the expression of disease phenotypes caused by CEP290 mutations. The BBSome binds to the N-terminal region of CEP290 through BBS4 and co-localizes with CEP290 to the transition zone (TZ) of primary cilia and centriolar satellites in ciliated cells, as well as to the connecting cilium in photoreceptor cells. Although CEP290 still localizes to the TZ and connecting cilium in BBSome-depleted cells, its localization to centriolar satellites is disrupted and CEP290 appears to disperse throughout the cytoplasm in BBSome-depleted cells. Genetic interactions were tested using Cep290(rd16)- and Bbs4-null mutant mouse lines. Additional loss of Bbs4 alleles in Cep290(rd16/rd16) mice results in increased body weight and accelerated photoreceptor degeneration compared with mice without Bbs4 mutations. Furthermore, double-heterozygous mice (Cep290(+/rd16);Bbs4(+/-)) have increased body weight compared with single-heterozygous animals. Our data indicate that genetic interactions between BBSome components and CEP290 could underlie the variable expression and overlapping phenotypes of ciliopathies caused by CEP290 mutations.
Mutation Phenotype Retina - metabolism Body Weight Bardet-Biedl Syndrome - metabolism Microtubule-Associated Proteins - genetics Microtubule-Associated Proteins - metabolism Humans Neoplasm Proteins - metabolism HEK293 Cells Antigens, Neoplasm - metabolism Bardet-Biedl Syndrome - genetics Neoplasm Proteins - genetics Nuclear Proteins - genetics Binding Sites Disease Models, Animal Antigens, Neoplasm - genetics Cell Line Mice, Transgenic Nuclear Proteins - metabolism Cilia - metabolism Animals Photoreceptor Cells - metabolism Mice Centrioles - metabolism Retina - pathology

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