Bo Yan
Liang Lou
Xi Lin
Tao Yu
Shuting Wu
Qing Lu
Wei Liu
Zhibin Huang
Mingjie Zhang
Wenqing Zhang
Zilong Wen
aDivision of Life Science and State Key Laboratory of Molecular Neuroscience, Center of Systems Biology and Human Health, The Hong Kong University of Science and Technology, Clearwater Bay, Kowloon, Hong Kong, China
bShanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China
cBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, 200240, China
dDepartment of Developmental Biology, School of Basic Medical Sciences, South China University of Technology, Guangzhou, 510630, China
eDivision of Life Science, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, China
More InformationCorresponding author: E-mail address: bo.yan@shphc.org.cn (Bo Yan);E-mail address: mczhangwq@scut.edu.cn (Wenqing Zhang);E-mail address: zilong@ust.hk (Zilong Wen)
Received Date: 2018-11-01
Accepted Date:2019-06-17
Rev Recd Date:2019-06-17
Available Online: 2019-06-22 Publish Date:2019-06-20
Abstract
Abstract
Microglia are tissue-resident macrophages residing in the central nervous system (CNS) and play critical roles in removing cellular debris and infectious agents as well as regulating neurogenesis and neuronal activities. Yet, the molecular basis underlying the establishment of microglia pool and the maintenance of their homeostasis in the CNS remain largely undefined. Here we report the identification and characterization of a mutant zebrafish, which harbors a point mutation in the nucleotide-binding oligomerization domain (NOD) like receptor gene nlrc3-like, resulting in the loss of microglia in a temperature sensitive manner. Temperature shift assay reveals that the late onset of nlrc3-like deficiency leads to excessive microglia cell death. Further analysis shows that the excessive microglia death in nlrc3-like deficient mutants is attributed, at least in part, to aberrant activation of canonical inflammasome pathway. Our study indicates that proper regulation of inflammasome cascade is critical for the maintenance of microglia homeostasis.Keywords: Zebrafish,
Microglia,
Inflammasome,
NOD-like receptors
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