A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\miltGD8116

General Information
SymbolDmel\miltGD8116SpeciesD. melanogaster
NameFlyBase IDFBal0210074
Feature typealleleAssociated geneDmel\milt
Map ( GBrowse ) GBrowse View Helpdetailed view
Allele class
Mutagenin vitro construct - RNAiin vitro construct - regulatory fusion
hide Recent Updates
Description
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Update Feed
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates Click here to see a list of all updates to this record from FB2010_08 and on.
hide Nature of the Allele
Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
RNAi reagent
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Scer\UAS regulatory sequences drive expression of an inverted repeat.
Carried in construct
Associated Sequence Features
Cytology
hide Phenotypic Data
hide Phenotypic Class
hide Phenotype Manifest In
hide Detailed Description
Statement
Reference
Expression of milt[GD8116] in eyes under the control of Scer\GAL4[GMR.PF] results in loss of mitochondria in the synaptic terminals of photoreceptor neurons in 3 day old flies. In addition, the presynaptic terminals contain vesicles with a wider range of sizes than in controls. No axonal or presynaptic neurodegeneration is detected in the lamina of these flies at 3 day old, but degeneration is seen in the lamina at 20 days, and more strongly at 30 days. When milt[GD8116] is expressed under the control of both Scer\GAL4[GMR.PF] and Scer\GAL4[elav-C155] neuronal degeneration is seen in 21 day-old flies, with the most prominent degeneration in the optic lobe. No degeneration is seen in the laminae of 30-day old wild type flies.
Glial cells show mis-distribution of mitochondria in third instar larvae expressing milt[GD8116] under the simultaneous control of both Scer\GAL4[repo.PL] and Scer\GAL4[repo].
Neuronal knockdown of milt by milt[GD8116] driven by Scer\GAL4[elav-C155] does not affect locomotor function up to 10 days after eclosion, but causes locomotor dysfunction after 17 days.
hide External Data
Linkouts
Bristle Screen Database - A database for RNAi phenotypes in bristle and notum development
hide Interactions
hide Phenotypic Class
hideSuppressed by
Statement
Reference
hideEnhancer of
Statement
Reference
hideNOT Enhancer of
Statement
Reference
hideOther
Statement
Reference
hide Phenotype Manifest In
hideSuppressed by
Statement
Reference
hideNOT suppressed by
Statement
Reference
hideEnhancer of
Statement
Reference
hideNOT Enhancer of
Statement
Reference
hideOther
Statement
Reference
hide Additional Comments
hide Genetic Interactions
Statement
Reference
Co-expression of par-1[Scer\UAS.T:Hsap\MYC] and milt[GD8116] under the control of Scer\GAL4[GMR.PF] causes prominent neurodegeneration in the lamina at 3 days old. Expression of tau[HM05101] suppresses the neurodegeneration seen in the lamina of 30 day old flies when milt[GD8116] is expressed under the control of Scer\GAL4[GMR.PF]. Expression of par-1[dsRNA.Scer\UAS.cMDa] suppresses the neurodegeneration seen in the lamina of 30 day old flies when milt[GD8116] is expressed under the control of Scer\GAL4[GMR.PF].
hide Xenogenetic Interactions
Statement
Reference
Expression of milt[GD8116] dramatically enhances neurodegeneration in the lamina of 3 day old flies expressing Hsap\MAPT[Scer\UAS.cWa] under the control of Scer\GAL4[GMR.PF] and as in flies expressing milt[GD8116] alone, there is a reduction in the number of mitochondria in the synaptic terminals of photoreceptor neurons. Expression of milt[GD8116] enhances the defects in axon pathology seen when Hsap\MAPT[Scer\UAS.cWa] is expressed under the control of Scer\GAL4[GMR.PF]. No neurofibrillary tangles seen in these flies. This enhancement is suppressed upon co-expression of par-1[dsRNA.Scer\UAS.cMDa]. Expression of milt[GD8116] does not enhance neurodegeneration in the lamina of 3 day old flies expressing Hsap\MAPT[Scer\UAS.S262A] under the control of Scer\GAL4[GMR.PF].
hide Complementation & Rescue Data
Comments
hide Stocks ( 2 )
VDRC
hide Notes on Origin
Discoverer
hide External Crossreferences & Linkouts
Other Crossreferences
Linkouts
Bristle Screen Database - A database for RNAi phenotypes in bristle and notum development
hide Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym
miltGD8116
 
Name Synonym
Secondary FlyBase IDs
hide References ( 5 )
Research paper
Iijima-Ando et al., 2012, PLoS Genet. 8(8): e1002918
Loss of Axonal Mitochondria Promotes Tau-Mediated Neurodegeneration and Alzheimer's Disease-Related Tau Phosphorylation Via PAR-1. [FBrf0219369]
Schmidt et al., 2012, J. Neurosci. 32(22): 7466--7476
Kinesin heavy chain function in Drosophila glial cells controls neuronal activity. [FBrf0218491]
Iijima-Ando et al., 2009, PLoS ONE 4(12): e8310
Mitochondrial mislocalization underlies Abeta42-induced neuronal dysfunction in a Drosophila model of Alzheimer's disease. [FBrf0209556]
Supplementary material
Mummery-Widmer et al., 2009, Nature 458(7241):
Supplementary Table 2 - Genome-wide bristle screen results. [FBrf0214518]
Personal communication to FlyBase
Dickson et al., 2007.7.18, RNAi construct and insertion data submitted by the Vienna Drosophila RNAi Center
RNAi construct and insertion data submitted by the Vienna Drosophila RNAi Center [FBrf0200327]