Signaling mechanism for synapse formation and function regulated by the release of GPI-anchored synaptogenic factors from astrocytes

NIH RePORTER · NIH · R01 · $333,594 · view on reporter.nih.gov ↗

Abstract

Dynamic interplay between neurons and glia is critical to establish the proper structure and function of the nervous system. In particular, astrocytes are powerful regulators of the multiple steps of synapse development and function. However, we lack mechanistic understanding of how signaling molecules are delivered from astrocytes to neurons to regulate the synaptogenesis. In this proposal, we present evidence that GDE3, the major regulator of the glycosylphosphatidylinositol (GPI)-anchored proteins on the astrocyte surface, is required for synapse development and function. GDE3 facilitates the release of GPI-anchored proteins from astrocytes in two modes: GPI-shedding and extracellular vesicular release. In this proposal, we will define the release mechanism of the active form of synaptogenic factors and downstream effectors of GDE3. Importantly, we will determine the specific role of GPI-anchorage in synapse development and function in the developing brain. Our results will reveal a novel signaling mechanism of astrocyte-neuron communications and aid the design of alternative therapeutic interventions for diseases caused by synaptogenic defects.

Key facts

NIH application ID
10188651
Project number
5R01NS102444-05
Recipient
UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
Principal Investigator
Sung Jin Park
Activity code
R01
Funding institute
NIH
Fiscal year
2021
Award amount
$333,594
Award type
5
Project period
2017-07-01 → 2023-06-30