Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 115, Issue 24, Pages 6303-6308Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1722613115
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Funding
- National Research, Development, and Innovation Office of Hungary [KTIA_NAP_13-2-2015-0003, KTIA_NAP_13-2-2014-0017, 2017-1.2.1-NKP-2017-00002, K_120391, FIEK_16-1-2016-0005, VEKOP-2.3.3-15-2016-00007]
- Bolyai Janos fellowship of the Hungarian Academy of Sciences
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C1q, a member of the immune complement cascade, is implicated in the selective pruning of synapses by microglial phagocytosis. C1q-mediated synapse elimination has been shown to occur during brain development, while increased activation and complement-dependent synapse loss is observed in neurodegenerative diseases. However, the molecular mechanisms underlying C1q-controlled synaptic pruning are mostly unknown. This study addresses distortions in the synaptic proteome leading to C1q-tagged synapses. Our data demonstrated the preferential localization of C1q to the presynapse. Proteomic investigation and pathway analysis of C1q-tagged synaptosomes revealed the presence of apoptotic-like processes in C1qtagged synapses, which was confirmed experimentally with apoptosis markers. Moreover, the induction of synaptic apoptotic-like mechanisms in a model of sensory deprivation-induced synaptic depression led to elevated C1q levels. Our results unveiled that C1q label-based synaptic pruning is triggered by and directly linked to apoptotic-like processes in the synaptic compartment.
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