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Author (up) Driscoll, M.; Gerstbrein, B. file  url
openurl 
  Title Dying for a cause: invertebrate genetics takes on human neurodegeneration Type Journal Article
  Year 2003 Publication Nature Reviews. Genetics Abbreviated Journal Nat Rev Genet  
  Volume 4 Issue 3 Pages 181-194  
  Keywords Alzheimer Disease/genetics/pathology; Animals; Animals, Genetically Modified; Caenorhabditis elegans/cytology/genetics; Cell Death; Drosophila melanogaster/cytology/genetics; Humans; Hypoxia/genetics/pathology; Invertebrates/cytology/*genetics; Ion Channels/metabolism; Models, Neurological; Mutation; Nerve Degeneration/*genetics/*pathology; Neurons/drug effects/pathology; Parkinson Disease/genetics/pathology; Peptides/genetics  
  Abstract If invertebrate neurons are injured by hostile environments or aberrant proteins they die much like human neurons, indicating that the powerful advantages of invertebrate molecular genetics might be successfully used for testing specific hypotheses about human neurological diseases, for drug discovery and for non-biased screens for suppressors and enhancers of neurodegeneration. Recent molecular dissection of the genetic requirements for hypoxia, excitotoxicity and death in models of Alzheimer disease, polyglutamine-expansion disorders, Parkinson disease and more, is providing mechanistic insights into neurotoxicity and suggesting new therapeutic interventions. An emerging theme is that neuronal crises of distinct origins might converge to disrupt common cellular functions, such as protein folding and turnover.  
  Call Number Serial 1706  
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Author (up) Frank, C.A. file  url
openurl 
  Title Homeostatic plasticity at the Drosophila neuromuscular junction Type Journal Article
  Year 2014 Publication Neuropharmacology Abbreviated Journal Neuropharmacology  
  Volume 78 Issue Pages 63-74  
  Keywords Animals; Drosophila melanogaster; Homeostasis; Neuromuscular Junction/*metabolism; *Neuronal Plasticity; Synapses/*metabolism; Ca(V)2; Calcium; Calcium channels; Calcium influx; Drosophila; Electrophysiology; Excitability; Genetics; Glutamate receptors; Homeostasis; Homeostatic neuroplasticity; Imaging; Molecular mechanism; Nmj; Neuromuscular junction; Pharmacology; Postsynaptic; Presynaptic; Readily releasable pool; Retrograde signaling; Signaling; Synaptic homeostasis; Transsynaptic  
  Abstract In biology, homeostasis refers to how cells maintain appropriate levels of activity. This concept underlies a balancing act in the nervous system. Synapses require flexibility (i.e. plasticity) to adjust to environmental challenges. Yet there must also exist regulatory mechanisms that constrain activity within appropriate physiological ranges. An abundance of evidence suggests that homeostatic regulation is critical in this regard. In recent years, important progress has been made toward identifying molecules and signaling processes required for homeostatic forms of neuroplasticity. The Drosophila melanogaster third instar larval neuromuscular junction (NMJ) has been an important experimental system in this effort. Drosophila neuroscientists combine genetics, pharmacology, electrophysiology, imaging, and a variety of molecular techniques to understand how homeostatic signaling mechanisms take shape at the synapse. At the NMJ, homeostatic signaling mechanisms couple retrograde (muscle-to-nerve) signaling with changes in presynaptic calcium influx, changes in the dynamics of the readily releasable vesicle pool, and ultimately, changes in presynaptic neurotransmitter release. Roles in these processes have been demonstrated for several molecules and signaling systems discussed here. This review focuses primarily on electrophysiological studies or data. In particular, attention is devoted to understanding what happens when NMJ function is challenged (usually through glutamate receptor inhibition) and the resulting homeostatic responses. A significant area of study not covered in this review, for the sake of simplicity, is the homeostatic control of synapse growth, which naturally, could also impinge upon synapse function in myriad ways. This article is part of the Special Issue entitled 'Homeostatic Synaptic Plasticity'.  
  Call Number Serial 1253  
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Author (up) Ramachandran, P.; Budnik, V. file  url
openurl 
  Title Dissection of Drosophila larval body-wall muscles Type Journal Article
  Year 2010 Publication Cold Spring Harbor Protocols Abbreviated Journal Cold Spring Harb Protoc  
  Volume 2010 Issue 8 Pages pdb.prot5469  
  Keywords Animals; Dissection/*methods; Drosophila melanogaster/*anatomy & histology; Larva/anatomy & histology; Magnetics/instrumentation; Muscles/*anatomy & histology  
  Abstract Over the last two decades, the Drosophila larval neuromuscular junction has gained immense popularity as a model system for the study of synaptic development, function, and plasticity. With this model, it is easy to visualize synapses and manipulate the system genetically with a high degree of temporal and spatial control, which makes it ideal for resolving problems in synaptic physiology and development. A number of different techniques have been used to dissect third-instar larval preparations to expose the body-wall muscles. Here, we describe a procedure that uses magnetic chambers and pins to allow for fine control in spreading the larval body wall.  
  Call Number Serial 1321  
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Author (up) Van de Ven, W.J.; Creemers, J.W.; Roebroek, A.J. file  url
openurl 
  Title Furin: the prototype mammalian subtilisin-like proprotein-processing enzyme. Endoproteolytic cleavage at paired basic residues of proproteins of the eukaryotic secretory pathway Type Journal Article
  Year 1991 Publication Enzyme Abbreviated Journal Enzyme  
  Volume 45 Issue 5-6 Pages 257-270  
  Keywords Animals; Binding Sites; Catalysis; Cloning, Molecular; Drosophila melanogaster; Furin; Humans; Invertebrate Hormones/genetics/metabolism; Mice; Models, Molecular; Multigene Family; Protein Conformation; Protein Precursors/*metabolism; *Protein Processing, Post-Translational; Sequence Homology, Amino Acid; Substrate Specificity; Subtilisins/genetics/*metabolism  
  Abstract Furin, the translational product of the recently discovered fur gene, appears to be the first known mammalian member of the subtilisin family of serine proteases and the first known mammalian proprotein-processing enzyme with cleavage selectivity for paired basic amino acid residues. Structurally and functionally, it resembles the prohormone-processing enzyme, kexin (EC 3.4.21.61), which is encoded by the KEX2 gene of yeast Saccharomyces cerevisiae. Most likely, furin is primarily involved in the processing of precursors of proteins that are secreted via the constitutive secretory pathway. Here, we review the discovery of the fur gene and describe the isolation of cDNA clones corresponding to human and mouse fur and to two fur-like genes of Drosophila melanogaster, Dfur1 and Dfur2. We also compare the structural organization of the various deduced furin proteins to that of yeast kexin, and of other members of the subtilisin family of serine proteases. Furthermore, the biosynthesis of biologically active human and mouse furin is evaluated. Finally, the cleavage specificity for paired basic amino acid residues of human and mouse furin is demonstrated by the correct processing of the precursor for von Willebrand factor.  
  Call Number Serial 524  
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Author (up) Wieschaus, E.; Nusslein-Volhard, C.; Kluding, H. file  url
openurl 
  Title Kruppel, a gene whose activity is required early in the zygotic genome for normal embryonic segmentation Type Journal Article
  Year 1984 Publication Developmental Biology Abbreviated Journal Dev Biol  
  Volume 104 Issue 1 Pages 172-186  
  Keywords Abdomen/anatomy & histology; Alleles; Animals; Drosophila melanogaster/embryology/*genetics; Embryo, Nonmammalian/*physiology; Female; Gastrula/physiology; *Genes; Heterozygote; Homozygote; *Mutation; Thorax/anatomy & histology  
  Abstract Embryos homozygous for Kruppel die as late embryos with an altered segmentation pattern. In strong alleles the normal thoracic and anterior abdominal segments are replaced by a partial mirror image duplication of the posterior abdomen. Weak alleles cause smaller pattern deletions in the thorax and abdomen and are not associated with mirror image duplications. The altered segmentation pattern can be traced back to 12 min after the onset of gastrulation, when the shorter germ bands in homozygous Kr embryos provide a first indication of abnormal patterning. The mutant was mapped to position 107.6 at the tip of the right arm of the second chromosome, cytologically to bands 60F2-5. Analysis of homozygous deficiency embryos indicate that the phenotype produced by strong point mutations probably represents the amorphic condition. The requirement for Kr+ gene activity is strictly zygotic. Maternal dosage of Kr+ has no effect on the embryonic phenotype, nor does homozygosity for Kr prevent germ cells from making normal eggs capable of normal embryonic development when fertilized by wild-type sperm. The requirement for Kr+ seems restricted to embryogenesis. Homozygous clones induced in imaginal discs during larval development survive and develop normally and in vivo cultures established from homozygous embryos proliferate normally and metamorphose into adult structures of normal morphology.  
  Call Number Serial 294  
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