1. The retromer complex in development and disease.

    Development 142(14):2392 (2015) PMID 26199408

    The retromer complex is a multimeric protein complex involved in recycling proteins from endosomes to the trans-Golgi network or plasma membrane. It thus regulates the abundance and subcellular distribution of its cargo within cells. Studies using model organisms show that the retromer complex i...
  2. Impaired Mitochondrial Energy Production Causes Light-Induced Photoreceptor Degeneration Independent of Oxidative Stress.

    PLoS Biology 13(7):e1002197 (2015) PMID 26176594 PMCID PMC4503542

    Two insults often underlie a variety of eye diseases including glaucoma, optic atrophy, and retinal degeneration-defects in mitochondrial function and aberrant Rhodopsin trafficking. Although mitochondrial defects are often associated with oxidative stress, they have not been linked to Rhodopsin...
  3. Correction: the retromer complex is required for rhodopsin recycling and its loss leads to photoreceptor degeneration.

    PLoS Biology 13(5):e1002170 (2015) PMID 26020534 PMCID PMC4447419

    [This corrects the article DOI: 10.1371/journal.pbio.1001847.].
  4. Huntingtin functions as a scaffold for selective macroautophagy.

    Nature Cell Biology 17(3):262 (2015) PMID 25686248

    Selective macroautophagy is an important protective mechanism against diverse cellular stresses. In contrast to the well-characterized starvation-induced autophagy, the regulation of selective autophagy is largely unknown. Here, we demonstrate that Huntingtin, the Huntington disease gene product...
  5. Huntingtin functions as a scaffold for selective macroautophagy.

    Nature Cell Biology 17(3):262 (2015) PMID 25686248

    Selective macroautophagy is an important protective mechanism against diverse cellular stresses. In contrast to the well-characterized starvation-induced autophagy, the regulation of selective autophagy is largely unknown. Here, we demonstrate that Huntingtin, the Huntington disease gene product...
  6. Fruit flies in biomedical research.

    Genetics 199(3):639 (2015) PMID 25624315 PMCID PMC4349060

    Many scientists complain that the current funding situation is dire. Indeed, there has been an overall decline in support in funding for research from the National Institutes of Health and the National Science Foundation. Within the Drosophila field, some of us question how long this funding cru...
  7. A voltage-gated calcium channel regulates lysosomal fusion with endosomes and autophagosomes and is required for neuronal homeostasis.

    PLoS Biology 13(3):e1002103 (2015) PMID 25811491 PMCID PMC4374850

    Autophagy helps deliver sequestered intracellular cargo to lysosomes for proteolytic degradation and thereby maintains cellular homeostasis by preventing accumulation of toxic substances in cells. In a forward mosaic screen in Drosophila designed to identify genes required for neuronal function ...
  8. Huntingtin functions as a scaffold for selective macroautophagy.

    Nature Cell Biology 17(3):262 (2015) PMID 25686248 PMCID PMC4344873

    Selective macroautophagy is an important protective mechanism against diverse cellular stresses. In contrast to the well-characterized starvation-induced autophagy, the regulation of selective autophagy is largely unknown. Here, we demonstrate that Huntingtin, the Huntington disease gene product...
  9. Fruit flies in biomedical research.

    Genetics 199(3):639 (2015) PMID 25624315 PMCID PMC4349060

    Many scientists complain that the current funding situation is dire. Indeed, there has been an overall decline in support in funding for research from the National Institutes of Health and the National Science Foundation. Within the Drosophila field, some of us question how long this funding cru...
  10. Huntingtin functions as a scaffold for selective macroautophagy.

    Nature Cell Biology 17(3):262 (2015) PMID 25686248 PMCID PMC4344873

    Selective macroautophagy is an important protective mechanism against diverse cellular stresses. In contrast to the well-characterized starvation-induced autophagy, the regulation of selective autophagy is largely unknown. Here, we demonstrate that Huntingtin, the Huntington disease gene product...
  11. Glial Lipid Droplets and ROS Induced by Mitochondrial Defects Promote Neurodegeneration.

    Cell 160(1-2):177 (2015) PMID 25594180

    Reactive oxygen species (ROS) and mitochondrial defects in neurons are implicated in neurodegenerative disease. Here, we find that a key consequence of ROS and neuronal mitochondrial dysfunction is the accumulation of lipid droplets (LD) in glia. In Drosophila, ROS triggers c-Jun-N-terminal Kina...
  12. Glial Lipid Droplets and ROS Induced by Mitochondrial Defects Promote Neurodegeneration.

    Cell 160(1-2):177 (2015) PMID 25594180

    Reactive oxygen species (ROS) and mitochondrial defects in neurons are implicated in neurodegenerative disease. Here, we find that a key consequence of ROS and neuronal mitochondrial dysfunction is the accumulation of lipid droplets (LD) in glia. In Drosophila, ROS triggers c-Jun-N-terminal Kina...
  13. Glial lipid droplets and ROS induced by mitochondrial defects promote neurodegeneration.

    Cell 160(1-2):177 (2015) PMID 25594180

    Reactive oxygen species (ROS) and mitochondrial defects in neurons are implicated in neurodegenerative disease. Here, we find that a key consequence of ROS and neuronal mitochondrial dysfunction is the accumulation of lipid droplets (LD) in glia. In Drosophila, ROS triggers c-Jun-N-terminal Kina...
  14. Glial Lipid Droplets and ROS Induced by Mitochondrial Defects Promote Neurodegeneration.

    Cell 160(1-2):177 (2015) PMID 25594180 PMCID PMC4377295

    Reactive oxygen species (ROS) and mitochondrial defects in neurons are implicated in neurodegenerative disease. Here, we find that a key consequence of ROS and neuronal mitochondrial dysfunction is the accumulation of lipid droplets (LD) in glia. In Drosophila, ROS triggers c-Jun-N-terminal Kina...
  15. A library of MiMICs allows tagging of genes and reversible, spatial and temporal knockdown of proteins in Drosophila.

    eLife 4 (2015) PMID 25824290 PMCID PMC4379497

    Here, we document a collection of ∼7434 MiMIC (Minos Mediated Integration Cassette) insertions of which 2854 are inserted in coding introns. They allowed us to create a library of 400 GFP-tagged genes. We show that 72% of internally tagged proteins are functional, and that more than 90% can be i...
  16. A genetic toolkit for tagging intronic MiMIC containing genes.

    eLife 4 (2015) PMID 26102525 PMCID PMC4499919

    Previously, we described a large collection of Minos-Mediated Integration Cassettes (MiMICs) that contain two phiC31 recombinase target sites and allow the generation of a new exon that encodes a protein tag when the MiMIC is inserted in a codon intron (Nagarkar-Jaiswal et al., 2015). These modi...
  17. A TRPV Channel in Drosophila Motor Neurons Regulates Presynaptic Resting Ca(2+) Levels, Synapse Growth, and Synaptic Transmission.

    Neuron 84(4):764 (2014) PMID 25451193 PMCID PMC4254599

    Presynaptic resting Ca(2+) influences synaptic vesicle (SV) release probability. Here, we report that a TRPV channel, Inactive (Iav), maintains presynaptic resting [Ca(2+)] by promoting Ca(2+) release from the endoplasmic reticulum in Drosophila motor neurons, and is required for both synapse de...
  18. A TRPV channel in Drosophila motor neurons regulates presynaptic resting Ca2+ levels, synapse growth, and synaptic transmission.

    Neuron 84(4):764 (2014) PMID 25451193 PMCID PMC4254599

    Presynaptic resting Ca(2+) influences synaptic vesicle (SV) release probability. Here, we report that a TRPV channel, Inactive (Iav), maintains presynaptic resting [Ca(2+)] by promoting Ca(2+) release from the endoplasmic reticulum in Drosophila motor neurons, and is required for both synapse de...
  19. A TRPV channel in Drosophila motor neurons regulates presynaptic resting Ca2+ levels, synapse growth, and synaptic transmission.

    Neuron 84(4):764 (2014) PMID 25451193 PMCID PMC4254599

    Presynaptic resting Ca(2+) influences synaptic vesicle (SV) release probability. Here, we report that a TRPV channel, Inactive (Iav), maintains presynaptic resting [Ca(2+)] by promoting Ca(2+) release from the endoplasmic reticulum in Drosophila motor neurons, and is required for both synapse de...
  20. A TRPV channel in Drosophila motor neurons regulates presynaptic resting Ca2+ levels, synapse growth, and synaptic transmission.

    Neuron 84(4):764 (2014) PMID 25451193 PMCID PMC4254599

    Presynaptic resting Ca(2+) influences synaptic vesicle (SV) release probability. Here, we report that a TRPV channel, Inactive (Iav), maintains presynaptic resting [Ca(2+)] by promoting Ca(2+) release from the endoplasmic reticulum in Drosophila motor neurons, and is required for both synapse de...