期刊
JOURNAL OF CELL BIOLOGY
卷 221, 期 10, 页码 -出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.202201050
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资金
- National Institutes of Health [S10RR028859, R01GM110413]
- National Natural Science Foundation of China [32070698, 32100541]
- University of Georgia (UGA) CURO Research Assistantship for undergraduate researchers
The loss of Chlamydomonas ARL13 impedes BBSome-dependent protein transport, resulting in overlapping biochemical defects in arl13 and bbs mutant cilia.
The GTPase Arlin 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.
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