# Loss of Jedi-1 impairs microglia phagocytosis, resulting in reduced postnatal neurogenesis in the ventricular-subventricular zone.

> **NIH NIH F32** · TULANE UNIVERSITY OF LOUISIANA · 2022 · $76,802

## Abstract

Project Summary
Jedi-1 is an engulfment receptor that mediates phagocytic clearance of apoptotic sensory neurons by satellite
glia in the developing murine peripheral nervous system. The clearance of apoptotic debris is also critical for
the development and maintenance of the central nervous system (CNS), in particular for postnatal
neurogenesis. Neurogenesis relies on the coupling of neural stem/progenitor cell (NSPC) proliferation,
newborn neuron apoptosis, and clearance of the apoptotic debris. Critically, loss of phagocytosis hinders
neurogenesis. Using immunofluorescent labeling in brain sections from male and female wildtype (WT)
and Jedi-1 knockout mice (JKO) in the first week of postnatal life, we show that Jedi-1 is expressed in WT
microglia residing in the postnatal neurogenic niche, the ventricular-subventricular zone (V-SVZ), but absent in
the knockout. Therefore, we asked whether Jedi-1 expression in microglia contributes to this coupling and
thereby regulates neurogenesis. To test whether loss of Jedi-1 hinders microglial phagocytic ability, we
employed an in vitro engulfment assay and found that JKO microglia display a significant reduction in
engulfment relative to WT microglia. This finding was recapitulated by an accumulation of apoptotic cells in the
JKO V-SVZ, as shown by TUNEL assay. To determine whether loss of Jedi-1 and subsequent disruption of
microglial phagocytic ability impacts neural precursor proliferation, we performed an EdU pulse at postnatal
day 7 in vivo. Our findings demonstrate that JKO mice have fewer proliferating neural progenitors in the V-SVZ
relative to WT mice. Furthermore, JKO mice have reduced numbers of MASH1+ newborn neurons when
compared to those of WT mice. Together, these data support the hypothesis that postnatal neurogenesis is
maintained in part by Jedi-1-dependent microglial phagocytosis of apoptotic cells in the V-SVZ.

## Key facts

- **NIH application ID:** 10704464
- **Project number:** 7F32HD107930-02
- **Recipient organization:** TULANE UNIVERSITY OF LOUISIANA
- **Principal Investigator:** Vivianne E Morrison
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $76,802
- **Award type:** 7
- **Project period:** 2022-11-01 → 2024-02-29

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10704464

## Citation

> US National Institutes of Health, RePORTER application 10704464, Loss of Jedi-1 impairs microglia phagocytosis, resulting in reduced postnatal neurogenesis in the ventricular-subventricular zone. (7F32HD107930-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10704464. Licensed CC0.

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