- Neuroinflammation and Neurodegeneration Mechanisms
- Immune cells in cancer
- Neuroscience and Neuropharmacology Research
- Neurogenesis and neuroplasticity mechanisms
- MicroRNA in disease regulation
- Zebrafish Biomedical Research Applications
Shenzhen Bay Laboratory
2023-2025
Microglia are brain-resident macrophages capable of long-term maintenance through self-renewal. Yet the mechanism governing turnover and lifespan microglia remains unknown. In zebrafish, arise from two sources, rostral blood island (RBI) aorta-gonad-mesonephros (AGM). The RBI-derived born early but have a short diminish in adulthood, while AGM-derived emerge later adulthood. Here, we show that attenuation RBI is due to their less competitiveness for neuron-derived interleukin-34 (Il34)...
Microglia are brain-resident macrophages playing pivotal roles in CNS development and homeostasis. Yet, the cellular molecular basis governing microglia maintenance remain largely unknown. Here, via utilizing a visible conditional knockout allele of pu.1 gene (the master regulator for microglia/macrophage lineage development) to generate mosaic populations adult zebrafish, we show that while -deficient immediate viable, they less competitive chronically eliminated through Tp53-mediated cell...
Microglia are brain-resident macrophages playing pivotal roles in CNS development and homeostasis. Yet, the cellular molecular basis governing microglia maintenance remain largely unknown. Here, via utilizing a visible conditional knockout allele of pu.1 gene (the master regulator for microglia/macrophage lineage development) to generate mosaic populations adult zebrafish, we show that while -deficient immediate viable, they less competitive chronically eliminated through Tp53-mediated cell...
Abstract Microglia are brain-resident macrophages that play pivotal roles in CNS development and homeostasis. Yet, the cellular molecular basis governing microglia maintenance remain largely unknown. By using a visible conditional knockout strategy to generate mosaic zebrafish, we show deficient for Pu.1/Spi1b, master regulator development, less competitive chronically eliminated Tp53-dependent manner. Interestingly, when both Pu.1 Spi-b (the paralogue of also called Spi1a) defective,...