The zinc finger transcription factor Sall1 is required for the early developmental transition of microglia in mouse embryos

Earl Parker Scott, Emma Breyak, Ryuichi Nishinakamura, Yasushi Nakagawa

Research output: Contribution to journalArticlepeer-review

Abstract

Microglia play many critical roles in neural development. Recent single-cell RNA-sequencing studies have found diversity of microglia both across different stages and within the same stage in the developing brain. However, how such diversity is controlled during development is poorly understood. In this study, we first found the expression of the macrophage mannose receptor CD206 in early-stage embryonic microglia on mouse brain sections. This expression showed a sharp decline between E12.5 and E13.5 across the central nervous system. We next tested the roles of the microglia-expressed zinc finger transcription factor SALL1 in this early transition of gene expression. By deleting Sall1 specifically in microglia, we found that many microglia continued to express CD206 when it is normally downregulated. In addition, the mutant microglia continued to show less ramified morphology in comparison with controls even into postnatal stages. Thus, SALL1 is required for early microglia to transition into a more mature status during development.

Original languageEnglish (US)
Pages (from-to)1720-1733
Number of pages14
JournalGlia
Volume70
Issue number9
DOIs
StatePublished - Sep 2022

Bibliographical note

Funding Information:
This work was supported by grant to Yasushi Nakagawa from NIH R21 NS117978.

Publisher Copyright:
© 2022 The Authors. GLIA published by Wiley Periodicals LLC.

Keywords

  • CD206
  • development
  • embryos
  • microglia
  • Sall1

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural

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