A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\DgdsRNA.Scer\UAS

General Information
SymbolDmel\DgdsRNA.Scer\UASSpeciesD. melanogaster
NameFlyBase IDFBal0145086
Feature typealleleAssociated geneDmel\Dg
Allele class
Mutagenin vitro construct - regulatory fusionin vitro construct - RNAi
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Description
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FB2013_03
FB2013_02
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Construct: Scer\UAS regulatory sequences drives expression of a Dg hairpin loop (that should produce dsRNA when expressed).
Carried in construct
Cytology
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The mean amplitude of the evoked junctional current (EJC) is decreased by approximately 40% at the neuromuscular junction in larvae expressing Dg[dsRNA.Scer\UAS] under the control of Scer\GAL4[how-24B] compared to in controls. The miniature junctional current (mEJC) amplitude is not decreased in the mutant animals. Quantal content is reduced by approximately 40% in the mutant larvae. Expression of Dg[dsRNA.Scer\UAS] under the control of Scer\GAL4[elav.PU] does not significantly affect the mean amplitude of the mEJC or the quantal content at the larval neuromuscular junction.
Third instar larval muscle sarcomeres are significantly smaller in animals expressing Dg[dsRNA.Scer\UAS] under the control of Scer\GAL4[tub] compared to controls. There is no difference in the overall size of muscles in these animals, and no defects in muscle attachment. Third instar larval muscle sarcomeres are much more variable in size in animals expressing Dg[dsRNA.Scer\UAS] under the control of Scer\GAL4[how-24B] compared to controls at 25[o]C. Individual larvae show either small or larger sarcomeres in each muscle, and a combination of both small and large sarcomeres in a single muscle is not seen. There is no difference in the overall size of muscles in these animals, and no defects in muscle attachment. Third instar larval muscle sarcomeres are larger in animals expressing Dg[dsRNA.Scer\UAS] under the control of Scer\GAL4[how-24B] compared to controls at 30[o]C. There is no difference in the overall size of muscles in these animals, and no defects in muscle attachment. There is no effect on third instar larval muscle size or muscle sarcomere size in animals expressing Dg[dsRNA.Scer\UAS] under the control of Scer\GAL4[69B] compared to controls. Expression of Dg[dsRNA.Scer\UAS] under the control of Scer\GAL4[how-24B], Scer\GAL4[tub], or Scer\GAL4[69B] does not affect crawling behaviour of third instar larvae. There is significantly higher muscle membrane resistance in larvae expressing Dg[dsRNA.Scer\UAS] under the control of Scer\GAL4[how-24B] at either 25[o]C or 30[o]C compared to controls.
Flies expressing Dg[dsRNA.Scer\UAS] under the control of either Scer\GAL4[tub] or the muscle-specific driver Scer\GAL4[how-24B], show comparable climbing ability at the beginning of adult life to control flies. However, the ability of these animals to climb declines significantly faster over time compared to controls. By 12 days (when expression is driven by Scer\GAL4[tub]) or 20 days (when expression is driven by Scer\GAL4[how-24B]), age-dependent muscle degeneration is observed including loss of muscle fibre organisation, vacuolisation and the absence of some muscles. Retinal photoreceptor cells are not elongated in adult eyes expressing Dg[dsRNA.Scer\UAS] under the control of either Scer\GAL4[tub]. Expression of Dg[dsRNA.Scer\UAS] in the eye disc (under the control of Scer\GAL4[GMR.PU]), or in all glial cells (under the control of Scer\GAL4[repo.PU]), both result in photoreceptor axon targeting defects. Axons stop irregularly, making gaps in the normal termination zone of the lamina plexus, deviating from the path and bundling aberrantly. Expression of Dg[dsRNA.Scer\UAS] in the mesodermal tissue (under the control of Scer\GAL4[how-24B]) does not effect the axon termination process.
Expression of DgdsRNA.Scer\UAS under the control of Scer\GAL4αTub84B.PL results in a multi-layered follicle epithelium.
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The oocyte polarity defects seen when Ras85DΔC40B mutant clones are made in the posterior follicle cell layer are partially rescued by expression of DgdsRNA.Scer\UAS in the clone using Scer\GAL4Act and the 'MARCM' technique. The polarity defects of posterior follicle cells (PFCs) seen in Ras85DΔC40B mutant PFC clones are partially rescued by expression of DgdsRNA.Scer\UAS in the clone using Scer\GAL4Act and the 'MARCM' technique.
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Reported As
Symbol Synonym
DgdsRNA.Scer\UAS
 
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hide References ( 6 )
Research paper
Bogdanik et al., 2008, PLoS ONE 3(4): e2084
Muscle dystroglycan organizes the postsynapse and regulates presynaptic neurotransmitter release at the Drosophila neuromuscular junction. [FBrf0210237]
Haines et al., 2007, Mol. Biol. Cell 18(12): 4721--4730
Dystroglycan and protein O-mannosyltransferases 1 and 2 are required to maintain integrity of Drosophila larval muscles. [FBrf0204214]
Shcherbata et al., 2007, EMBO J. 26(2): 481--493
Dissecting muscle and neuronal disorders in a Drosophila model of muscular dystrophy. [FBrf0192541]
Poulton and Deng, 2006, Proc. Natl. Acad. Sci. U.S.A. 103(34): 12775--12780
Dystroglycan down-regulation links EGF receptor signaling and anterior-posterior polarity formation in the Drosophila oocyte. [FBrf0193906]
Schneider et al., 2006, Development 133(19): 3805--3815
Perlecan and Dystroglycan act at the basal side of the Drosophila follicular epithelium to maintain epithelial organization. [FBrf0192630]
Deng et al., 2003, Development 130(1): 173--184
Dystroglycan is required for polarizing the epithelial cells and the oocyte in Drosophila. [FBrf0151949]