@article{8f75dce0fca847beb2bea41f842e69df,
title = "RPGRIP1L helps to establish the ciliary gate for entry of proteins",
abstract = "Mutations in transition zone genes change the composition of the ciliary proteome.We isolated newmutations in RPGRIP1L (denotated as RPG1 in algae) that affect the localization of the transition zone protein NPHP4 in the model organism Chlamydomonas reinhardtii. NPHP4 localization is not affected in multiple new intraflagellar transport (IFT) mutants.We compared the proteome of cilia from wildtype and mutants that affect the transition zone (RPGRIP1L) or IFT (IFT172 and DHC1b) by mass spectrometry. The rpg1-1 mutant cilia show the most dramatic increase in cytoplasmic proteins. These nonciliary proteins function in translation, membrane remodeling, ATP production and as chaperonins. These proteins are excluded in isolated cilia from fla11-1 (IFT172) and fla24-1 (DHC1b). Our data support the idea that RPGRIP1L, but not IFT proteins, acts as part of the gate for cytoplasmic proteins. The rpg1-1 cilia lack only a few proteins, which suggests that RPGRIP1L only has a minor role of in the retention of ciliary proteins. The fla11-1 mutant shows the greatest loss/reduction of proteins, and one-third of these proteins have a transmembrane domain. Hence, IFT172 may play a role in the retention of proteins.",
keywords = "Basal body, Chlamydomonas reinhardtii, Cilia, Transition zone",
author = "Huawen Lin and Suyang Guo and Dutcher, {Susan K.}",
note = "Funding Information: This work is supported by a grant from the National Institute of General Medical Science to S.K.D. (NIH R01-GM32843). This publication is solely the responsibility of the authors and does not necessarily represent the official view of NCRR or NIH. Deposited in PMC for immediate release. Funding Information: We are extremely grateful to Dr Ursula Goodenough for suggesting that we examine the CC-4348 strain. We thank Nick Nauman for help during the initial mapping of the fla11-2 mutant in CC-4348 and Gervette Penny for many useful comments on the manuscript. Antibodies were provided by Dr Dennis Diener for POC2, by Dr Doug Cole for IFT172 and by Dr David Mitchell for CPC1. We thank the Genome Technology Access Center in the Department of Genetics at Washington University School of Medicine for help with genomic analysis. The Center is partially supported by NCI Cancer Center Support Grant #P30 CA91842 to the Siteman Cancer Center and by ICTS/CTSA Grant # UL1TR000448 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research. Publisher Copyright: {\textcopyright} 2018. Published by The Company of Biologists Ltd.",
year = "2018",
month = oct,
day = "1",
doi = "10.1242/jcs.220905",
language = "English",
volume = "131",
journal = "Journal of Cell Science",
issn = "0021-9533",
number = "20",
}