Journal
JOURNAL OF CELL BIOLOGY
Volume 187, Issue 7, Pages 1117-1132Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200909183
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Funding
- Diabetes Endocrinology Research Center [DK32520]
- National Institutes of Health [GM030626, DC006103, AR048898, AR048526, GM060992]
- Vermont Genetics Network through a National Institutes of Health [P20 RR16462]
- National Center for Research Resources
- Robert W. Booth Endowment
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In humans, seven evolutionarily conserved genes that cause the cilia-related disorder Bardet-Biedl syndrome (BBS) encode proteins that form a complex termed the BBSome. The function of the BBSome in the cilium is not well understood. We purified a BBSome-like complex from Chlamydomonas reinhardtii flagella and found that it contains at least BBS1, -4, -5, -7, and -8 and undergoes intraflagellar transport (IFT) in association with a subset of IFT particles. C. reinhardtii insertional mutants defective in BBS1, -4, and -7 assemble motile, full-length flagella but lack the ability to phototax. In the bbs4 mutant, the assembly and transport of IFT particles are unaffected, but the flagella abnormally accumulate several signaling proteins that may disrupt phototaxis. We conclude that the BBSome is carried by IFT but is an adapter rather than an integral component of the IFT machinery. C. reinhardtii BBS4 may be required for the export of signaling proteins from the flagellum via IFT.
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