Qki is an essential regulator of microglial phagocytosis in demyelination

Jiangong Ren, Congxin Dai, Xin Zhou, Joseph A. Barnes, Xi Chen, Yunfei Wang, Liang Yuan, Takashi Shingu, Amy B. Heimberger, Yiwen Chen, Jian Hu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


The mechanism underpinning the regulation of microglial phagocytosis in demyelinating diseases is unclear. Here, we showed that the Quaking protein (Qki) in microglia was greatly induced by demyelination in the brains of both mice and humans. Deletion of the Quaking gene (Qk) in microglia severely impaired the clearance of myelin debris. Transcriptomic profiling indicated that depletion of Qki impaired total RNA levels and splicing of the genes involved in phagosome formation and maturation. RNA immunoprecipitation (RIP) confirmed the physical interactions between the Qki protein and the mRNAs of Qki targets that are involved in phagocytosis, indicating that Qki regulates their RNA stability. Both Qki depletion and inhibition of Qki target Cd36 greatly reduced the phagocytic activity of microglia and macrophages. The defective uptake and degradation of myelin debris caused by Qki depletion in microglia resulted in unresolved myelin debris that impaired axon integrity, oligodendrocyte maturation, and subsequent remyelination. Thus, our results demonstrate that Qki is an essential regulator of microglia’s phagocytic activity under demyelinating conditions.

Original languageEnglish (US)
Article numbere20190348
JournalJournal of Experimental Medicine
Issue number1
StatePublished - Jan 4 2021

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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