P2ry12-CreER robustly and specifically labels microglia in fate-mapping and ribosomal profiling experiments, revealing new markers for myeloid subpopulations in the central nervous system.
Two novel subsets of microglia identified by their unique autofluorescence profiles differ in their subcellular organization, proteomic signatures and in their response to aging and lysosomal dysfunction.
Adult-born neurons in the olfactory bulb that develop in the absence of microglia have a higher density of small spines but weaker excitatory inputs and reduced responses to sensory stimuli.
TGFβ signaling to retinal microglia is central to the regulation of neuroinflammatory responses relevant to age-related macular degeneration (AMD), a leading cause of blindness in the developed world.
A combined approach of unbiased proteomics, biochemistry, genetics, and transgenic animal models reveals that GPR56/ADGRG1 regulates myelin formation and repair by interacting with its microglial-derived ligand transglutaminase 2.
During adult neurogenesis in the olfactory bulb, microglia regulate the elimination (pruning), formation, and maintenance of synapses on newborn neurons, contributing to the functional integrity of the olfactory bulb circuitry.
In mouse models of Rett Syndrome, global loss of the Mecp2 gene induces microglia to engulf excess synapses, while microglia-specific loss or gain of Mecp2 has little impact on disease.
