A G-protein activation cascade from Arl13B to Arl3 and 1 implications for ciliary targeting of lipidated proteins

نویسندگان

  • Katja Gotthardt
  • Mandy Lokaj
  • Carolin Koerner
  • Nathalie Falk
  • Andreas Gießl
چکیده

27 28 29 Small G-proteins of the ADP-ribosylation-factor-like (Arl) subfamily have been shown to be 30 crucial to ciliogenesis and cilia maintenance. Active Arl3 is involved in targeting and

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A G-protein activation cascade from Arl13B to Arl3 and implications for ciliary targeting of lipidated proteins

Small G-proteins of the ADP-ribosylation-factor-like (Arl) subfamily have been shown to be crucial to ciliogenesis and cilia maintenance. Active Arl3 is involved in targeting and releasing lipidated cargo proteins from their carriers PDE6δ and UNC119a/b to the cilium. However, the guanine nucleotide exchange factor (GEF) which activates Arl3 is unknown. Here we show that the ciliary G-protein A...

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Structural insights into the small G-protein Arl13B and implications for Joubert syndrome.

Ciliopathies are human diseases arising from defects in primary or motile cilia. The small G-protein Arl13B (ADP-ribosylation factor-like 13B) localizes to microtubule doublets of the ciliary axoneme and is mutated in Joubert syndrome. Its GDP/GTP mechanistic cycle and the effect of its mutations in patients with Joubert syndrome remain elusive. In the present study we applied high resolution s...

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Structural basis for Arl3-specific release of myristoylated ciliary cargo from UNC119.

Access to the ciliary membrane for trans-membrane or membrane-associated proteins is a regulated process. Previously, we have shown that the closely homologous small G proteins Arl2 and Arl3 allosterically regulate prenylated cargo release from PDEδ. UNC119/HRG4 is responsible for ciliary delivery of myristoylated cargo. Here, we show that although Arl3 and Arl2 bind UNC119 with similar affinit...

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Ciliary membrane proteins traffic through the Golgi via a Rabep1/GGA1/Arl3-dependent mechanism

Primary cilia contain specific receptors and channel proteins that sense the extracellular milieu. Defective ciliary function causes ciliopathies such as autosomal dominant polycystic kidney disease (ADPKD). However, little is known about how large ciliary transmembrane proteins traffic to the cilia. Polycystin-1 (PC1) and -2 (PC2), the two ADPKD gene products, are large transmembrane proteins ...

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تاریخ انتشار 2015