Loss of ARL13 impedes BBSome-dependent cargo export from Chlamydomonas cilia

Author:

Dai Jin1ORCID,Zhang Gui1,Alkhofash Rama A.1,Mekonnen Betlehem1,Saravanan Sahana1,Xue Bin2,Fan Zhen-Chuan2ORCID,Betleja Ewelina3,Cole Douglas G.3,Liu Peiwei4ORCID,Lechtreck Karl1ORCID

Affiliation:

1. Cellular Biology, University of Georgia, Athens, GA 1

2. State Key Laboratory of Food Nutrition and Safety, Institute of Health Biotechnology, Tianjin University of Science and Technology, Tianjin, China 2

3. Biological Sciences, University of Idaho, Moscow, ID 3

4. College of Life Science, Shandong Normal University, Jinan, Shandong, China 4

Abstract

The GTPase Arl13b participates in ciliary protein transport, but its contribution to intraflagellar transport (IFT), the main motor-based protein shuttle of cilia, remains largely unknown. Chlamydomonas arl13 mutant cilia were characterized by both abnormal reduction and accumulation of select membrane-associated proteins. With respect to the latter, a similar set of proteins including phospholipase D (PLD) also accumulated in BBSome-deficient cilia. IFT and BBSome traffic were apparently normal in arl13. However, transport of PLD, which in control cells moves by BBSome-dependent IFT, was impaired in arl13, causing PLD to accumulate in cilia. ARL13 only rarely and transiently traveled by IFT, indicating that it is not a co-migrating adapter securing PLD to IFT trains. In conclusion, the loss of Chlamydomonas ARL13 impedes BBSome-dependent protein transport, resulting in overlapping biochemical defects in arl13 and bbs mutant cilia.

Funder

National Institutes of Health

National Natural Science Foundation of China

University of Georgia

Publisher

Rockefeller University Press

Subject

Cell Biology

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