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Branch-restricted localization of phosphatase Prl-1 specifies axonal synaptogenesis domains
Olivier Urwyler1,2, Azadeh Izadifar3,4, Sofie Vandenbogaerde3
1VIB Center for Brain and Disease Research, Leuven, Belgium. dietmar.schmucker@kuleuven.vib.be olivier.urwyler@uzh.ch.
Science (New York, N.Y.)
|May 4, 2019
Summary
The phosphatase of regenerating liver (Prl-1) protein controls synapse formation in fruit fly neurons. Prl-1
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- Central nervous system (CNS) development requires precise control over synapse formation and abundance.
- Subcellular regulation of synaptogenesis is crucial for proper neural circuit function.
Purpose of the Study:
- To investigate the role of the phosphatase of regenerating liver (Prl-1) as an axon-intrinsic factor in synapse formation.
- To elucidate the mechanisms by which Prl-1 regulates synaptogenesis in a spatially restricted manner.
Main Methods:
- Utilized *Drosophila* melanogaster as a model organism.
- Investigated Prl-1 function in mechanosensory neurons.
- Examined the effects of Prl-1 loss-of-function and overexpression on presynapse number and localization.
- Analyzed the modulation of insulin receptor (InR) signaling pathway by Prl-1.
- Studied the role of untranslated regions of *prl-1* mRNA in Prl-1 localization and function.
Main Results:
- Loss of Prl-1 reduced presynapse number and altered terminal arbor organization in mechanosensory neuron axon collaterals.
- Flies lacking Prl-1 exhibited locomotor defects.
- Prl-1 overexpression led to the formation of ectopic synapses.
- Prl-1 compartmentalizes and modulates insulin receptor (InR) signaling within specific axon compartments to control synapse number.
- Axon branch-specific localization and function of Prl-1 are dependent on its mRNA's untranslated regions.
Conclusions:
- Prl-1 acts as an axon-intrinsic factor that promotes synapse formation in a spatially restricted manner.
- Compartmentalized restriction of Prl-1 is a key mechanism for subcellular control of axonal synaptogenesis.
- Prl-1's regulation of InR signaling within specific axon domains is critical for controlling synapse abundance.
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