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Phylogenetic profiling and cellular analyses of ARL16 reveal roles in traffic of IFT140 and INPP5E

SI. Dewees, R. Vargová, KR. Hardin, RE. Turn, S. Devi, J. Linnert, U. Wolfrum, T. Caspary, M. Eliáš, RA. Kahn

. 2022 ; 33 (4) : ar33. [pub] 20220223

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc22019026

Grantová podpora
F31 HD096815 NICHD NIH HHS - United States
R35 GM122549 NIGMS NIH HHS - United States
R35 GM122568 NIGMS NIH HHS - United States

E-zdroje Online Plný text

NLK Free Medical Journals od 1992 do Před 2 měsíci
PubMed Central od 1992 do Před 2 měsíci
Europe PubMed Central od 1992 do Před 2 měsíci
Open Access Digital Library od 1989-11-01
Open Access Digital Library od 1997-01-01

Odkazy

PubMed 35196065
DOI 10.1091/mbc.e21-10-0509-t
Knihovny.cz E-zdroje

The ARF family of regulatory GTPases is ancient, with 16 members predicted to have been present in the last eukaryotic common ancestor. Our phylogenetic profiling of paralogues in diverse species identified four family members whose presence correlates with that of a cilium/flagellum: ARL3, ARL6, ARL13, and ARL16. No prior evidence links ARL16 to cilia or other cell functions, despite its presence throughout eukaryotes. Deletion of ARL16 in mouse embryonic fibroblasts (MEFs) results in decreased ciliogenesis yet increased ciliary length. We also found Arl16 knockout (KO) in MEFs to alter ciliary protein content, including loss of ARL13B, ARL3, INPP5E, and the IFT-A core component IFT140. Instead, both INPP5E and IFT140 accumulate at the Golgi in Arl16 KO lines, while other intraflagellar transport (IFT) proteins do not, suggesting a specific defect in traffic from Golgi to cilia. We propose that ARL16 regulates a Golgi-cilia traffic pathway and is required specifically in the export of IFT140 and INPP5E from the Golgi.

Citace poskytuje Crossref.org

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