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Published on: April 12, 2020
MAGED1 stabilizes NEUROD1 to promote Per3 expression in the pineal gland
Shengye Xu1, Jing Dai2, Tianyi Jiang1
1Department of Neurobiology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, 211166, Jiangsu, China.
Aims:
The molecular mechanisms that regulate Per3 expression in the pineal gland remain incompletely understood. This study aimed to determine whether MAGED1 regulates pineal Per3 expression and to define the intermediary mechanism linking MAGED1 to transcriptional control of Per3.
Materials And Methods:
Maged1 knockout mice and cultured cells were used to examine the relationship among MAGED1, NEUROD1, and Per3. Immunofluorescence, RNA fluorescence in situ hybridization, western blotting, proximity ligation assays, co-immunoprecipitation, ubiquitination assays, chromatin immunoprecipitation-qPCR, and luciferase reporter assays were performed to assess protein localization, protein-protein interaction, NEUROD1 stability, and Per3 promoter activity.
Key Findings:
MAGED1 showed time-of-day-dependent subcellular localization in the mouse pineal gland, with increased nuclear accumulation during the dark phase. Loss of Maged1 reduced pineal Per3 mRNA abundance and decreased NEUROD1 protein levels. MAGED1 did not show detectable enrichment at the Per3 promoter but interacted with NEUROD1 in pineal tissue and cultured cells. Mechanistically, MAGED1 maintained NEUROD1 protein abundance by limiting ubiquitin-mediated proteasomal degradation. NEUROD1 directly activated the Per3 promoter, and disruption of the MAGED1-NEUROD1 interaction reduced Per3 promoter activity.
Significance:
These findings identify a MAGED1-NEUROD1-Per3 regulatory pathway in the pineal gland and provide a molecular mechanism by which MAGED1 supports pineal Per3 transcription.
