MassIVE MSV000089424

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CFAP418 participates in membrane-associated cellular processes through binding lipids during ciliogenesis

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Description

iliopathies and retinal degenerative diseases are heterogeneous groups of genetic diseases. CFAP418 is a causative gene of both diseases, and its sequence is evolutionarily conserved. Here, we employ affinity purification coupled with mass spectrometry and quantitative lipidomic, proteomic, and phosphoproteomic approaches to address the function of CFAP418 in retinas. We show CFAP418 unexpectedly binds to lipid metabolism precursor phosphatidic acid (PA) and mitochondrion-specific lipid cardiolipin but does not form a tight and static complex with proteins. Loss of Cfap418 leads to a widespread disruption of membrane lipid homeostasis and changes in protein-membrane association, which subsequently causes mitochondrial morphological and functional defects and membrane remodeling abnormalities in multiple vesicular trafficking pathways. The signaling of PA-binding protein kinase Ca is increased. Our results indicate that membrane lipid imbalance is a new pathological mechanism underlying inherited ciliopathies and retinal degenerations, which is associated with other known causative RAB28 and BBS genes. [doi:10.25345/C54B2X84N] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: photoreceptor ; retinal degeneration ; cardiolipin ; phosphatic acid

Contact

Principal Investigators:
(in alphabetical order) 		Jun Yang, Moran Eye Center, University of Utah, USA
Submitting User: JunYang

Publications

Clark AM, Yu D, Neiswanger G, Zhu D, Zou J, Maschek JA, Burgoyne T, Yang J.
Disruption of CFAP418 interaction with lipids causes widespread abnormal membrane-associated cellular processes in retinal degenerations.
JCI Insight. Epub 2024 Jan 9.

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