Yumei Wu

Focal dopaminergic axon swellings in the dorsolateral striatum of Synj1 R259Q mutant mice are clusters of DAT-rich, onion-like plasma membrane invaginations, and the same region shows reduced evoked dopamine release.

The paper identifies BLTP3A as a protein associated with late endocytic membranes and shows it interacts with the CASM pathway to respond to lysosome damage.

The paper shows that DDHD2 is essential for neurons to use fatty acids from lipid droplets as an energy source during activity when glucose is unavailable.

This paper identifies RAB1A and ARFGAP1-positive membranes as essential for autophagosome biogenesis, interacting with ATG2A to support lipid transport during autophagosome formation.

This study identifies interactions that mediate BLTP2 localization at ER-PM contacts and shows its role in controlling plasma membrane dynamics through lipid transport.

The paper shows that expressing a synaptopodin construct in non-neuronal cells generates ER stacks resembling the spine apparatus, revealing a role for synaptopodin-dependent actin matrix in their formation.

This study identifies VPS13B's localization at the cis-trans Golgi interface and shows its functional interaction with FAM177A1 in lipid transport and Golgi dynamics.

The paper shows that synaptophysin and synaptogyrin family proteins co-express with synapsin to generate small vesicles and that their absence leads to larger synaptic vesicles.

This study investigates how a mutation in Synaptojanin-1 affects ciliary properties in iPSC-derived dopaminergic neurons, revealing impaired protein clearance and altered Ca2+ channel distribution.

This study shows that mutations in synaptojanin1 and auxilin synergistically worsen dopaminergic axonal pathology in mice, suggesting a role in Parkinson's disease pathogenesis.

The paper shows that ATG9A forms distinct vesicle phases from synaptic vesicle proteins within synapsin condensates in fibroblasts and nerve terminals.

The paper investigates synaptopodin's properties and identifies its protein neighbors in dendritic spines, suggesting the spine apparatus matrix functions as a liquid condensate.

The paper shows that combining a Parkinson's disease mutation in synaptojanin 1 with Sac2 knockout in mice leads to severe neurological defects, suggesting Sac2 as a PD risk gene.