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Publication : EMC3 Is Essential for Retinal Organization and Neurogenesis During Mouse Retinal Development.

First Author  Cao X Year  2021
Journal  Invest Ophthalmol Vis Sci Volume  62
Issue  2 Pages  31
PubMed ID  33605987 Mgi Jnum  J:302526
Mgi Id  MGI:6507803 Doi  10.1167/iovs.62.2.31
Citation  Cao X, et al. (2021) EMC3 Is Essential for Retinal Organization and Neurogenesis During Mouse Retinal Development. Invest Ophthalmol Vis Sci 62(2):31
abstractText  Purpose: We used a mouse model to explore the role of the endoplasmic reticulum membrane protein complex subunit 3 (EMC3) in mammalian retinal development. Methods: The transcription pattern of Emc3 in C57BL/6 mice was analyzed by in situ hybridization. To explore the effects of EMC3 absence on retinal development, the Cre-loxP system was used to generate retina-specific Emc3 in knockout mice (Emc3flox/flox, Six3-cre+; CKO). Morphological changes in the retina of E13.5, E17.5, P0.5, and P7 mice were observed via hematoxylin and eosin staining. Immunofluorescence staining was used to assess protein distribution and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining to assess apoptosis changes. Proteins were identified and quantified by Western blotting and proteomic analysis. Electroretinogram (ERG), fundus color photography, and optical coherence tomography were performed on 5-week-old mice to evaluate retinal function and structure. Results: The Emc3 mRNA was widely distributed in the whole retina during development. Loss of retinal EMC3 led to retinal rosette degeneration with mislocalization of cell junction molecules (beta-catenin, N-cadherin, and zonula occludens-1) and polarity molecules (Par3 and PKCzeta). Endoplasmic reticulum stress and TUNEL apoptosis signals were present in retinal rosette-forming cells. Although the absence of EMC3 promoted the production of photoreceptor cells, 5-week-old mice lost all visual function and had severe retinal morphological degeneration. Conclusions: EMC3 regulates retinal structure by maintaining the polarity of retinal progenitor cells and regulating retinal cell apoptosis.
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