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The Oligodendrocyte Transcription Factor 2 OLIG2 regulates transcriptional repression during myelinogenesis in rodents

Author

Listed:
  • Kunkun Zhang

    (Xiamen University
    the First Affiliated Hospital of Xiamen University
    Xiamen University)

  • Shaoxuan Chen

    (Xiamen University
    the First Affiliated Hospital of Xiamen University
    Xiamen University)

  • Qihua Yang

    (Xiamen University)

  • Shuanghui Guo

    (Xiamen University)

  • Qiang Chen

    (Xiamen University
    the First Affiliated Hospital of Xiamen University
    Xiamen University)

  • Zhixiong Liu

    (Xiamen University
    the First Affiliated Hospital of Xiamen University
    Xiamen University)

  • Li Li

    (Xiamen University)

  • Mengyun Jiang

    (Xiamen University)

  • Hongda Li

    (Xiamen University)

  • Jin Hu

    (Xiamen University)

  • Xu Pan

    (Xiamen University, Xiamen)

  • Wenbo Deng

    (the First Affiliated Hospital of Xiamen University)

  • Naian Xiao

    (Xiamen University
    the First Affiliated Hospital of Xiamen University)

  • Bo Wang

    (Xiamen University)

  • Zhan-xiang Wang

    (Xiamen University
    the First Affiliated Hospital of Xiamen University)

  • Liang Zhang

    (Xiamen University
    the First Affiliated Hospital of Xiamen University
    Xiamen University)

  • Wei Mo

    (Xiamen University
    the First Affiliated Hospital of Xiamen University
    Xiamen University)

Abstract

OLIG2 is a transcription factor that activates the expression of myelin-associated genes in the oligodendrocyte-lineage cells. However, the mechanisms of myelin gene inactivation are unclear. Here, we uncover a non-canonical function of OLIG2 in transcriptional repression to modulate myelinogenesis by functionally interacting with tri-methyltransferase SETDB1. Immunoprecipitation and chromatin-immunoprecipitation assays show that OLIG2 recruits SETDB1 for H3K9me3 modification on the Sox11 gene, which leads to the inhibition of Sox11 expression during the differentiation of oligodendrocytes progenitor cells (OPCs) into immature oligodendrocytes (iOLs). Tissue-specific depletion of Setdb1 in mice results in the hypomyelination during development and remyelination defects in the injured rodents. Knockdown of Sox11 by siRNA in rat primary OPCs or depletion of Sox11 in the oligodendrocyte lineage in mice could rescue the hypomyelination phenotype caused by the loss of OLIG2. In summary, our work demonstrates that the OLIG2-SETDB1 complex can mediate transcriptional repression in OPCs, affecting myelination.

Suggested Citation

  • Kunkun Zhang & Shaoxuan Chen & Qihua Yang & Shuanghui Guo & Qiang Chen & Zhixiong Liu & Li Li & Mengyun Jiang & Hongda Li & Jin Hu & Xu Pan & Wenbo Deng & Naian Xiao & Bo Wang & Zhan-xiang Wang & Lian, 2022. "The Oligodendrocyte Transcription Factor 2 OLIG2 regulates transcriptional repression during myelinogenesis in rodents," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
  • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-29068-z
    DOI: 10.1038/s41467-022-29068-z
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