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A postsynaptic PI3K-cII dependent signaling controller for presynaptic homeostatic plasticity.

Anna G Hauswirth1,2, Kevin J Ford1,2, Tingting Wang1,2

  • 1Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, United States.

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|January 6, 2018
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Summary

Presynaptic homeostatic plasticity (PHP) stabilizes neural connections. Researchers identified key proteins, including PI3K-cII, PI3K-cIII, and Rab11, crucial for PHP

Keywords:
D. melanogasterendosomehomeostatic plasticitymembrane traffickingneuromuscular junctionneuroscienceneurotransmissionsystems biology

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Presynaptic homeostatic plasticity (PHP) is vital for stabilizing synaptic transmission across species.
  • PHP's molecular mechanisms, particularly postsynaptic signaling, are not fully understood.

Purpose of the Study:

  • To identify the molecular components of the postsynaptic machinery regulating PHP.
  • To elucidate the roles of specific signaling molecules in PHP.

Main Methods:

  • An electrophysiology-based screen of the *Drosophila* kinome and phosphatome.
  • Localization studies of key proteins using microscopy.
  • Functional assays to assess the role of identified proteins in PHP.

Main Results:

  • Identified a postsynaptic signaling platform involving Phosphoinositide 3-kinase (PI3K)-cII, PI3K-cIII, and the small GTPase Rab11, essential for PHP.
  • PI3K-cII localizes to Golgi-derived vesicles and is required for generating PI(3)P, which recruits Rab11 to recycling endosomes.
  • A distinct postsynaptic platform subdivision acts as a controller for retrograde trans-synaptic signaling.

Conclusions:

  • The study defines a novel postsynaptic signaling platform critical for PHP.
  • This platform, involving PI3K-cII, PI3K-cIII, and Rab11, regulates synaptic stability through retrograde signaling.