Author
Listed:
- Thomas A. Ray
(Duke University School of Medicine
Duke University School of Medicine)
- Kelly Cochran
(Duke University School of Medicine
Duke University School of Medicine)
- Chris Kozlowski
(Duke University School of Medicine
Duke University School of Medicine)
- Jingjing Wang
(Duke University School of Medicine
Duke University School of Medicine)
- Graham Alexander
(Duke University)
- Martha A. Cady
- William J. Spencer
- Philip A. Ruzycki
(John F. Hardesty, M.D. Department of Ophthalmology and Visual Sciences, Washington University)
- Brian S. Clark
(John F. Hardesty, M.D. Department of Ophthalmology and Visual Sciences, Washington University
Washington University)
- Annelies Laeremans
(Advanced Cell Diagnostics)
- Ming-Xiao He
(Advanced Cell Diagnostics)
- Xiaoming Wang
(Advanced Cell Diagnostics)
- Emily Park
(Advanced Cell Diagnostics)
- Ying Hao
(Duke University School of Medicine)
- Alessandro Iannaccone
(Duke University School of Medicine)
- Gary Hu
(Duke University School of Medicine
Duke University School of Medicine)
- Olivier Fedrigo
(Duke University
The Rockefeller University)
- Nikolai P. Skiba
(Duke University School of Medicine)
- Vadim Y. Arshavsky
(Duke University School of Medicine)
- Jeremy N. Kay
(Duke University School of Medicine
Duke University School of Medicine)
Abstract
Genes encoding cell-surface proteins control nervous system development and are implicated in neurological disorders. These genes produce alternative mRNA isoforms which remain poorly characterized, impeding understanding of how disease-associated mutations cause pathology. Here we introduce a strategy to define complete portfolios of full-length isoforms encoded by individual genes. Applying this approach to neural cell-surface molecules, we identify thousands of unannotated isoforms expressed in retina and brain. By mass spectrometry we confirm expression of newly-discovered proteins on the cell surface in vivo. Remarkably, we discover that the major isoform of a retinal degeneration gene, CRB1, was previously overlooked. This CRB1 isoform is the only one expressed by photoreceptors, the affected cells in CRB1 disease. Using mouse mutants, we identify a function for this isoform at photoreceptor-glial junctions and demonstrate that loss of this isoform accelerates photoreceptor death. Therefore, our isoform identification strategy enables discovery of new gene functions relevant to disease.
Suggested Citation
Thomas A. Ray & Kelly Cochran & Chris Kozlowski & Jingjing Wang & Graham Alexander & Martha A. Cady & William J. Spencer & Philip A. Ruzycki & Brian S. Clark & Annelies Laeremans & Ming-Xiao He & Xiao, 2020.
"Comprehensive identification of mRNA isoforms reveals the diversity of neural cell-surface molecules with roles in retinal development and disease,"
Nature Communications, Nature, vol. 11(1), pages 1-20, December.
Handle:
RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-17009-7
DOI: 10.1038/s41467-020-17009-7
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Cited by:
- Raphaël Dos Reis & Etienne Kornobis & Alyssa Pereira & Frederic Tores & Judit Carrasco & Candice Gautier & Céline Jahannault-Talignani & Patrick Nitschké & Christian Muchardt & Andreas Schlosser & Han, 2022.
"Complex regulation of Gephyrin splicing is a determinant of inhibitory postsynaptic diversity,"
Nature Communications, Nature, vol. 13(1), pages 1-17, December.
- Arpiar Saunders & Kee Wui Huang & Cassandra Vondrak & Christina Hughes & Karina Smolyar & Harsha Sen & Adrienne C. Philson & James Nemesh & Alec Wysoker & Seva Kashin & Bernardo L. Sabatini & Steven A, 2022.
"Ascertaining cells’ synaptic connections and RNA expression simultaneously with barcoded rabies virus libraries,"
Nature Communications, Nature, vol. 13(1), pages 1-18, December.
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