Kiel G. Ormerod

This study shows that pathogenic huntingtin in Drosophila muscle causes protein aggregation, nuclear and mitochondrial dysfunction, and impaired neuromuscular performance without overt structural changes.

This study identifies kinesin 1 and 3 as critical regulators of organelle trafficking in motor neurons, leading to morphological and functional disruptions in neuromuscular junctions and behavior.

This study tracks the progression of pathogenic huntingtin protein aggregates and their physiological impacts in a Drosophila model of Huntington's Disease.

This study shows that muscle-specific disruption of the Drosophila sallimus gene affects neuromuscular junction formation and function, leading to altered sarcomere structure and locomotory behavior.

The paper shows disruption of Ca2+ oscillations in Drosophila perineurial glia leads to seizure-like behavior without affecting BBB structure.

This study investigates how tonic and phasic motoneurons in Drosophila respond to activity changes or ablation, showing distinct structural and functional plasticity.

This study shows that glial Ca2+ signaling regulates neuronal excitability through K+ buffering via calcineurin-dependent endocytosis and K2P channel expression in Drosophila.