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

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 membr...

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Detalles Bibliográficos
Autores principales: Dai, Jin, Zhang, Gui, Alkhofash, Rama A., Mekonnen, Betlehem, Saravanan, Sahana, Xue, Bin, Fan, Zhen-Chuan, Betleja, Ewelina, Cole, Douglas G., Liu, Peiwei, Lechtreck, Karl
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Rockefeller University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9436004/
https://www.ncbi.nlm.nih.gov/pubmed/36040375
http://dx.doi.org/10.1083/jcb.202201050
Descripción
Sumario: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.