Chapter title |
Binary Function of ARL3-GTP Revealed by Gene Knockouts
|
---|---|
Chapter number | 39 |
Book title |
Retinal Degenerative Diseases
|
Published in |
Advances in experimental medicine and biology, January 2018
|
DOI | 10.1007/978-3-319-75402-4_39 |
Pubmed ID | |
Book ISBNs |
978-3-31-975401-7, 978-3-31-975402-4
|
Authors |
Christin Hanke-Gogokhia, Jeanne M. Frederick, Houbin Zhang, Wolfgang Baehr, Hanke-Gogokhia, Christin, Frederick, Jeanne M., Zhang, Houbin, Baehr, Wolfgang |
Abstract |
UNC119 and PDEδ are lipid-binding proteins and are thought to form diffusible complexes with transducin-α and prenylated OS proteins, respectively, to mediate their trafficking to photoreceptor outer segments. Here, we investigate mechanisms of trafficking which are controlled by Arf-like protein 3 (Arl3), a small GTPase. The activity of ARL3 is regulated by a GEF (ARL13b) and a GAP (RP2). In a mouse germline knockout of RP2, ARL3-GTP is abundant as its intrinsic GTPase activity is extremely low. High levels of ARL3-GTP impair binding and trafficking of cargo to the outer segment. Germline knockout of ARL3 is embryonically lethal generating a syndromic ciliopathy-like phenotype. Retina- and rod-specific knockout of ARL3 allow to determine the precise mechanisms leading to photoreceptor degeneration. The knockouts reveal binary functions of ARL3-GTP as a key molecule in late-stage photoreceptor ciliogenesis and cargo displacement factor. |
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