Dion K. Dickman

The paper compares glutamate receptor expression in larval and adult Drosophila muscles, finding differences in subunit composition and extrasynaptic expression of GluCl.

The paper shows RIM is not universally required for neurotransmission but acts as a specialized factor enhancing high-release synapses.

The paper performs a CRISPR screen in Drosophila to identify genes involved in presynaptic homeostatic plasticity, finding Ekar as a critical regulator.

The paper introduces GCaMP8 variants targeted to synaptic compartments and develops CaFire software to quantify Ca2+ signals, showing improved sensitivity and resolution compared to existing methods.

The paper shows that presynaptic release probability, not synaptic strength, decreases with sleep loss and affects sleep need across species.

The paper investigates how two distinct motor inputs contribute to presynaptic homeostatic plasticity (PHP) in Drosophila, showing input-specific mechanisms for stabilizing neuromuscular junction activity.

This paper identifies Insomniac as a Cul3 adaptor protein that regulates sleep and synaptic homeostasis in Drosophila, linking Cul3 dysfunction to autism and schizophrenia.

The paper develops a CRISPR toolkit for tissue-specific gene knockout in Drosophila motor neurons, muscles, and glial cells, revealing ESCRT's role in NMJ extracellular vesicle formation.

The paper identifies physiological and nanoscale differences in glutamatergic synapses between tonic and phasic neurons at the Drosophila neuromuscular junction.

The paper shows that transsynaptic nanocolumn rings rapidly modulate during homeostatic plasticity to stabilize synaptic efficacy.

This study uses botulinum neurotoxin to isolate neurotransmission from tonic and phasic neurons in Drosophila, revealing heterosynaptic plasticity rules.

This study shows that excess glutamate release selectively regulates GluR subtypes through competition and Ca2+ signaling in Drosophila.

This paper develops a hybrid chemical-genetic voltage reporter for voltage imaging in Drosophila, enabling selective neuron labeling and voltage monitoring in intact tissues.

The paper identifies distinct target-specific mechanisms that stabilize synaptic strength at pre- and post-synaptic compartments in Drosophila neuromuscular junctions.

The paper investigates how synaptic strength is maintained in Drosophila larvae arrested in development, finding that presynaptic homeostatic depression compensates for excessive synaptic growth.

This study identifies the sleep gene insomniac as essential for retrograde homeostatic signaling by ubiquitinating targets at postsynaptic densities in Drosophila.

The paper screens Drosophila genes affecting synaptic growth and identifies three mechanisms that stabilize synaptic strength despite growth changes.

The paper identifies a molecular mechanism for presynaptic plasticity involving rapid remodeling of active zone modules, which sustains neurotransmitter release potentiation over time.

The paper uses CRISPR to tag Ca2+ channels in Drosophila and shows they are differentially regulated during presynaptic homeostatic potentiation and depression.

The paper uses ribosome profiling in Drosophila to show post-translational mechanisms drive retrograde signaling in presynaptic efficacy, with no transcriptional or translational changes required.

This study identifies Esyt as a presynaptic ER Ca2+ sensor that enhances neurotransmission and synaptic growth in Drosophila.