PUBLICATION

dock8 deficiency attenuates microglia colonization in early zebrafish larvae

Authors
Wu, L., Xue, R., Chen, J., Xu, J.
ID
ZDB-PUB-220819-1
Date
2022
Source
Cell death discovery   8: 366 (Journal)
Registered Authors
Chen, Jiahao, Wu, Linxiu, Xue, Rongtao, Xu, Jin
Keywords
none
MeSH Terms
none
PubMed
35977943 Full text @ Cell Death Discov
Abstract
Microglia are tissue-resident macrophages that carry out immune functions in the brain. The deficiency or dysfunction of microglia has been implicated in many neurodegenerative disorders. DOCK8, a member of the DOCK family, functions as a guanine nucleotide exchange factor and plays key roles in immune regulation and neurological diseases. The functions of DOCK8 in microglia development are not fully understood. Here, we generated zebrafish dock8 mutants by CRISPR/Cas9 genome editing and showed that dock8 mutations attenuate microglia colonization in the zebrafish midbrain at early larvae stages. In vivo time-lapse imaging revealed that the motility of macrophages was reduced in the dock8 mutant. We further found that cdc42/cdc42l, which encode the small GTPase activated by Dock8, also regulate microglia colonization in zebrafish. Collectively, our study suggests that the Dock8-Cdc42 pathway is required for microglia colonization in zebrafish larvae.
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Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping