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Papers of the Week

Papers: 16 Mar 2024 - 22 Mar 2024

2024 Mar 18

Cell Rep




PRRC2B modulates oligodendrocyte progenitor cell development and myelination by stabilizing Sox2 mRNA.


Zhang Y, Song Z, Wu R, Kong X, Zhang H, Li S, Gong X, Gong S, Cheng J, Yuan F, Wu H, Wang S, Yuan Z


Oligodendrocyte progenitor cells (OPCs) differentiate into myelin-producing cells and modulate neuronal activity. Defects in OPC development are associated with neurological diseases. N-methyladenosine (mA) contributes to neural development; however, the mechanism by which mA regulates OPC development remains unclear. Here, we demonstrate that PRRC2B is an mA reader that regulates OPC development and myelination. Nestin-Cre-mediated Prrc2b deletion affects neural stem cell self-renewal and glial differentiation. Moreover, the oligodendroglia lineage-specific deletion of Prrc2b reduces the numbers of OPCs and oligodendrocytes, causing hypomyelination and impaired motor coordination. Integrative methylated RNA immunoprecipitation sequencing, RNA sequencing, and RNA immunoprecipitation sequencing analyses identify Sox2 as the target of PRRC2B. Notably, PRRC2B, displaying separate and cooperative functions with PRRC2A, stabilizes mRNA by binding to mA motifs in the coding sequence and 3′ UTR of Sox2. In summary, we identify the posttranscriptional regulation of PRRC2B in OPC development, extending the understanding of PRRC2 family proteins and providing a therapeutic target for myelin-related disorders.