PUBLICATION

Pu.1/Spi1 dosage controls the turnover and maintenance of microglia in zebrafish and mammals

Authors
Wu, Y., Guo, W., Kuang, H., Wu, X., Trinh, T.H., Wang, Y., Zhao, S., Wen, Z., Yu, T.
ID
ZDB-PUB-250718-1
Date
2025
Source
eLIFE   14: (Journal)
Registered Authors
YU, Tao
Keywords
cell competition, developmental biology, maintenance, microglia, mouse, pu.1 dosage, turnover, zebrafish
Datasets
GEO:GSE283170
MeSH Terms
  • Microglia*/cytology
  • Microglia*/metabolism
  • Proto-Oncogene Proteins*/metabolism
  • Zebrafish*
  • Male
  • Trans-Activators*/metabolism
  • Mice
  • Mammals/metabolism
  • Animals
PubMed
40673490 Full text @ Elife
Abstract
Microglia are brain-resident macrophages playing pivotal roles in central nervous system (CNS) development and homeostasis. Yet, the cellular and molecular basis governing microglia maintenance remains largely unknown. Here, by utilizing a visible conditional knockout allele of pu.1/spi1b gene (the master regulator for microglia/macrophage lineage development) to generate mosaic microglia populations in adult zebrafish, we show that while pu.1-deficient microglia are immediately viable, they are less competitive, and chronically eliminated through Tp53-mediated cell competition. Interestingly, when conditionally inactivating Pu.1 in adult spi-b (the orthologue of mouse Spi-b) null mutants, microglia are rapidly depleted via apoptosis, suggesting that Pu.1 and Spi-b regulate microglia maintenance in a dosage-dependent manner. The dosage-dependent regulation of microglia maintenance by PU.1/SPI1 is evolutionarily conserved in mice, as shown by conditionally inactivating single and both Spi1 alleles in microglia, respectively. Collectively, our study reveals the conserved cellular and molecular mechanisms controlling microglia turnover and maintenance in teleosts and mammals.
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