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Cell-surface proteomic profiling identifies CD72 as a regulator of microglial tiling.
Tamara C Chan1,2,3,4, Mohit Rastogi2,3, Micah X Williams2,3,4
1Neurosciences Interdepartmental Program, Stanford University School of Medicine, CA, USA.
Biorxiv : the Preprint Server for Biology
|June 12, 2025
Summary
Microglial tiling, a sign of brain health, is disrupted by CD72. This study identifies CD72 as a key regulator of microglial spacing and function, offering new insights into brain homeostasis.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglial tiling, characterized by uniform spacing and non-overlapping processes, is a key indicator of central nervous system homeostasis.
- The underlying molecular mechanisms governing microglial tiling remain largely unknown.
Purpose of the Study:
- To identify cell-surface proteins involved in regulating microglial tiling.
- To investigate the functional role of candidate proteins in maintaining microglial spacing and homeostasis.
Main Methods:
- Utilized cell-surface proximity labeling and mass spectrometry to profile the microglial proteome.
- Employed single-cell RNA sequencing and functional imaging assays to screen candidate proteins.
- Validated findings using in vitro models and organotypic hippocampal brain slices.
Main Results:
- Identified CD72, a microglial expressed coreceptor, as a disruptor of microglial tiling.
- Demonstrated that CD72 modulates pathways critical for cell adhesion, repulsive signaling, microglial activation, and cytoskeletal organization.
- Validated CD72's role in both in vitro and in situ brain slice models.
Conclusions:
- CD72 plays a significant role in regulating microglial tiling and spacing.
- These findings provide a foundation for understanding the functional implications of microglial tiling in health and disease.
