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  • 1
    Online Resource
    Online Resource
    Nearly Neutral Secretory Vesicles in Drosophila Nerve Terminals
    Elsevier BV ; 2006
    In:  Biophysical Journal Vol. 90, No. 6 ( 2006-03), p. L45-L47
    Details
    In: Biophysical Journal, Elsevier BV, Vol. 90, No. 6 ( 2006-03), p. L45-L47
    Type of Medium: Online Resource
    ISSN: 0006-3495
    URL: Article
    DOI: 10.1529/biophysj.106.080978
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2006
    detail.hit.zdb_id: 1477214-0
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  • 2
    Online Resource
    Online Resource
    “A fly appeared”: sable , a classic Drosophila mutation, maps to Yippee , a gene affecting body color, wings, and bristles
    Oxford University Press (OUP) ; 2022
    In:  G3 Genes|Genomes|Genetics Vol. 12, No. 5 ( 2022-05-06)
    Details
    In: G3 Genes|Genomes|Genetics, Oxford University Press (OUP), Vol. 12, No. 5 ( 2022-05-06)
    Abstract: Insect body color is an easily assessed and visually engaging trait that is informative on a broad range of topics including speciation, biomaterial science, and ecdysis. Mutants of the fruit fly Drosophila melanogaster have been an integral part of body color research for more than a century. As a result of this long tenure, backlogs of body color mutations have remained unmapped to their genes, all while their strains have been dutifully maintained, used for recombination mapping, and part of genetics education. Stemming from a lesson plan in our undergraduate genetics class, we have mapped sable1, a dark body mutation originally described by Morgan and Bridges, to Yippee, a gene encoding a predicted member of the E3 ubiquitin ligase complex. Deficiency/duplication mapping, genetic rescue, DNA and cDNA sequencing, RT-qPCR, and 2 new CRISPR alleles indicated that sable1 is a hypomorphic Yippee mutation due to an mdg4 element insertion in the Yippee 5′-UTR. Further analysis revealed additional Yippee mutant phenotypes including curved wings, ectopic/missing bristles, delayed development, and failed adult emergence. RNAi of Yippee in the ectoderm phenocopied sable body color and most other Yippee phenotypes. Although Yippee remains functionally uncharacterized, the results presented here suggest possible connections between melanin biosynthesis, copper homeostasis, and Notch/Delta signaling; in addition, they provide insight into past studies of sable cell nonautonomy and of the genetic modifier suppressor of sable.
    Type of Medium: Online Resource
    ISSN: 2160-1836
    URL: Article
    DOI: 10.1093/g3journal/jkac058
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2629978-1
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  • 3
    Online Resource
    Online Resource
    Multipotent neural cell lines can engraft and participate in development of mouse cerebellum
    Elsevier BV ; 1992
    In:  Cell Vol. 68, No. 1 ( 1992-1), p. 33-51
    Details
    In: Cell, Elsevier BV, Vol. 68, No. 1 ( 1992-1), p. 33-51
    Type of Medium: Online Resource
    ISSN: 0092-8674
    URL: Article
    DOI: 10.1016/0092-8674(92)90204-P
    RVK:
    XA 36269
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1992
    detail.hit.zdb_id: 187009-9
    detail.hit.zdb_id: 2001951-8
    SSG: 12
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  • 4
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    Online Resource
    The Synaptic Protein Syntaxin1 Is Required for Cellularization of Drosophila Embryos
    Rockefeller University Press ; 1997
    In:  The Journal of Cell Biology Vol. 138, No. 4 ( 1997-08-25), p. 861-875
    Details
    In: The Journal of Cell Biology, Rockefeller University Press, Vol. 138, No. 4 ( 1997-08-25), p. 861-875
    Abstract: Syntaxins are membrane proteins involved in vesicle trafficking and are required for the release of neurotransmitter at nerve terminals. The presence of syntaxins on target membranes has been hypothesized to confer specificity to targeting and fusion via interactions with complementary vesicle-associated proteins, the synaptobrevins or VAMPS. We have mutagenized syntaxin1 in Drosophila and have found that it links the mechanism of synaptic transmission to a distinct cell biological process: the cellularization of early embryos. This specialized form of cell division separates the 6,000 nuclei of the syncytial blastoderm into separate cells through the invagination of the surface membrane of the embryo. During this process, syntaxin1 protein is present on the newly forming lateral cell surfaces and invaginating cleavage furrows. This protein is derived both from maternal deposition of mRNA and protein and from early zygotic transcription. To analyze syntaxin1's role in early development, female germ line mosaics mutant for syntaxin1 expression were generated by mitotic recombination to reduce the maternal contribution. Visualizing the actin cytoskeleton and glycosylated surface proteins reveals that embryos with insufficient syntaxin1 have large acellular patches. The patches do not appear until cellularization begins, and the process fails entirely within these regions. These results provide genetic evidence that membrane trafficking is required for the cellularization of the syncytial blastoderm. We propose that the invagination of the surface membrane proceeds by the fusion of intracellular membrane vesicles with the surface. This reaction uses the same syntaxin1 protein as is required for neurotransmitter secretion at synapses. Thus, a single syntaxin can participate in trafficking steps that are functionally as distinct as synaptic transmission and cell division.
    Type of Medium: Online Resource
    ISSN: 0021-9525 , 1540-8140
    URL: Article
    DOI: 10.1083/jcb.138.4.861
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1997
    detail.hit.zdb_id: 1421310-2
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  • 5
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    Online Resource
    Activity Induces Fmr1-Sensitive Synaptic Capture of Anterograde Circulating Neuropeptide Vesicles
    Society for Neuroscience ; 2016
    In:  The Journal of Neuroscience Vol. 36, No. 46 ( 2016-11-16), p. 11781-11787
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 36, No. 46 ( 2016-11-16), p. 11781-11787
    Abstract: Synaptic neuropeptide and neurotrophin stores are maintained by constitutive bidirectional capture of dense-core vesicles (DCVs) as they circulate in and out of the nerve terminal. Activity increases DCV capture to rapidly replenish synaptic neuropeptide stores following release. However, it is not known whether this is due to enhanced bidirectional capture. Here experiments at the Drosophila neuromuscular junction, where DCVs contain neuropeptides and a bone morphogenic protein, show that activity-dependent replenishment of synaptic neuropeptides following release is evident after inhibiting the retrograde transport with the dynactin disruptor mycalolide B or photobleaching DCVs entering a synaptic bouton by retrograde transport. In contrast, photobleaching anterograde transport vesicles entering a bouton inhibits neuropeptide replenishment after activity. Furthermore, tracking of individual DCVs moving through boutons shows that activity selectively increases capture of DCVs undergoing anterograde transport. Finally, upregulating fragile X mental retardation 1 protein (Fmr1, also called FMRP) acts independently of futsch/MAP-1B to abolish activity-dependent, but not constitutive, capture. Fmr1 also reduces presynaptic neuropeptide stores without affecting activity-independent delivery and evoked release. Therefore, presynaptic motoneuron neuropeptide storage is increased by a vesicle capture mechanism that is distinguished from constitutive bidirectional capture by activity dependence, anterograde selectivity, and Fmr1 sensitivity. These results show that activity recruits a separate mechanism than used at rest to stimulate additional synaptic capture of DCVs for future release of neuropeptides and neurotrophins. SIGNIFICANCE STATEMENT Synaptic release of neuropeptides and neurotrophins depends on presynaptic accumulation of dense-core vesicles (DCVs). At rest, DCVs are captured bidirectionally as they circulate through Drosophila motoneuron terminals by anterograde and retrograde transport. Here we show that activity stimulates further synaptic capture that is distinguished from basal capture by its selectivity for anterograde DCVs and its inhibition by overexpression of the fragile X retardation protein Fmr1. Fmr1 dramatically lowers DCV numbers in synaptic boutons. Therefore, activity-dependent anterograde capture is a major determinant of presynaptic peptide stores.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2212-16.2016
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2016
    detail.hit.zdb_id: 1475274-8
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  • 6
    Online Resource
    Online Resource
    Complex gene organization of synaptic protein SNAP-25 in Drosophila melanogaster
    Elsevier BV ; 1997
    In:  Gene Vol. 194, No. 2 ( 1997-07), p. 169-177
    Details
    In: Gene, Elsevier BV, Vol. 194, No. 2 ( 1997-07), p. 169-177
    Type of Medium: Online Resource
    ISSN: 0378-1119
    URL: Article
    DOI: 10.1016/S0378-1119(97)00106-6
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1997
    detail.hit.zdb_id: 1491012-3
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Dominant-negative NSF2 disrupts the structure and function ofdrosophila neuromuscular synapses
    Wiley ; 2002
    In:  Journal of Neurobiology Vol. 51, No. 4 ( 2002-06-15), p. 261-271
    Details
    In: Journal of Neurobiology, Wiley, Vol. 51, No. 4 ( 2002-06-15), p. 261-271
    Type of Medium: Online Resource
    ISSN: 0022-3034 , 1097-4695
    URL: Issue
    URL: Journal
    URL: Article
    DOI: 10.1002/neu.v51:4
    DOI: 10.1002/(ISSN)1097-4695
    DOI: 10.1002/neu.10059
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2002
    detail.hit.zdb_id: 1474900-2
    detail.hit.zdb_id: 2266191-8
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  • 8
    Online Resource
    Online Resource
    Presynaptic Ryanodine Receptor-Activated Calmodulin Kinase II Increases Vesicle Mobility and Potentiates Neuropeptide Release
    Society for Neuroscience ; 2007
    In:  The Journal of Neuroscience Vol. 27, No. 29 ( 2007-07-18), p. 7799-7806
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 27, No. 29 ( 2007-07-18), p. 7799-7806
    Abstract: Although it has been postulated that vesicle mobility is increased to enhance release of transmitters and neuropeptides, the mechanism responsible for increasing vesicle motion in nerve terminals and the effect of perturbing this mobilization on synaptic plasticity are unknown. Here, green fluorescent protein-tagged dense-core vesicles (DCVs) are imaged in Drosophila motor neuron terminals, where DCV mobility is increased for minutes after seconds of activity. Ca 2+ -induced Ca 2+ release from presynaptic endoplasmic reticulum (ER) is shown to be necessary and sufficient for sustained DCV mobilization. However, this ryanodine receptor (RyR)-mediated effect is short-lived and only initiates signaling. Calmodulin kinase II (CaMKII), which is not activated directly by external Ca 2+ influx, then acts as a downstream effector of released ER Ca 2+ . RyR and CaMKII are essential for post-tetanic potentiation of neuropeptide secretion. Therefore, the presynaptic signaling pathway for increasing DCV mobility is identified and shown to be required for synaptic plasticity.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1879-07.2007
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2007
    detail.hit.zdb_id: 1475274-8
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  • 9
    Online Resource
    Online Resource
    Distinct Requirements for Evoked and Spontaneous Release of Neurotransmitter Are Revealed by Mutations in the Drosophila Gene neuronal-synaptobrevin
    Society for Neuroscience ; 1998
    In:  The Journal of Neuroscience Vol. 18, No. 6 ( 1998-03-15), p. 2028-2039
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 18, No. 6 ( 1998-03-15), p. 2028-2039
    Abstract: Two modes of vesicular release of transmitter occur at a synapse: spontaneous release in the absence of a stimulus and evoked release that is triggered by Ca 2+ influx. These modes often have been presumed to represent the same exocytotic apparatus functioning at different rates in different Ca 2+ concentrations. To investigate the mechanism of transmitter release, we have examined the role of synaptobrevin/VAMP, a protein involved in vesicular docking and/or fusion. We generated a series of mutations, including null mutations, in neuronal-synaptobrevin ( n-syb ), the neuronally expressed synaptobrevin gene in Drosophila . Mutant embryos completely lacking n-syb form morphologically normal neuromuscular junctions. Electrophysiological recordings from the neuromuscular junction of these mutants reveal that the excitatory synaptic current evoked by stimulation of the motor neuron is abolished entirely. However, spontaneous release of quanta from these terminals persists, although its rate is reduced by 75%. Thus, at least a portion of the spontaneous “minis” that are seen at the synapse can be generated by a protein complex that is distinct from that required for an evoked synaptic response.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.18-06-02028.1998
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1998
    detail.hit.zdb_id: 1475274-8
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  • 10
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    Online Resource
    Selective Effects of neuronal-synaptobrevin Mutations on Transmitter Release Evoked by Sustained Versus Transient Ca 2+ Increases and by cAMP
    Society for Neuroscience ; 1999
    In:  The Journal of Neuroscience Vol. 19, No. 7 ( 1999-04-01), p. 2432-2441
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 19, No. 7 ( 1999-04-01), p. 2432-2441
    Abstract: Synaptobrevin is a key constituent of the synaptic vesicle membrane. The neuronal-synaptobrevin ( n - syb ) gene in Drosophila is essential for nerve-evoked synaptic currents, but miniature excitatory synaptic currents (mESCs) remain even in the complete absence of this gene. To further characterize the defect in these mutants, we have examined conditions that stimulate secretion. Despite the inability of an action potential to trigger fusion, high K + saline could increase the frequency of mESCs 4- to 17-fold in a Ca 2+ -dependent manner, and the rate of fusion approached 25% of that seen in wild-type synapses under the same conditions. Similarly, the mESC frequency in n-syb null mutants could be increased by a Ca 2+ ionophore, A23187, and by black widow spider venom. Thus, the ability of the vesicles to fuse in response to sustained increases in cytosolic Ca 2+ persisted in the absence of this protein. Tetanic stimulation could also increase the frequency of mESCs, particularly toward the end of a train and after the train of stimuli. In contrast, these mutants did not respond to an elevation of cAMP induced by an activator of adenylyl cyclase, forskolin, or a membrane-permeable analog of cAMP, dibutyryl cAMP, which in wild-type synapses causes a marked increase in the mESC frequency even in the absence of external Ca 2+ . These results are discussed in the context of models that invoke a special role for n-syb in coupling fusion to the transient, local changes in Ca 2+ and an as yet unidentified target of cAMP.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.19-07-02432.1999
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1999
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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