A Database of Drosophila Genes & Genomes

FB2012_01, released January 20th, 2012
 

Allele Dmel\mys1

General Information
SymbolDmel\mys1SpeciesD. melanogaster
NameFlyBase IDFBal0012678
Feature typealleleAssociated geneDmel\mys
Allele classamorphic allele - genetic evidence, loss of function allele
Mutagen32P
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Description
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FB2012_01
Controlled Vocabulary Terms
References
Unknown
FB2011_10
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Deletion of at least 1kb beginning in central portion of coding region and extending towards 3' of gene, probably beyond the 3' end of the gene. Faint residual band on immunoblots (as for Df(1)C128) where product is thought to be a remnant from the maternal supply.
Cytology
Polytene chromosomes normal.
 
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Statement
Reference
The somatic muscles are detached and shrunken in stage 16 homozygous embryos. These detached muscles do not show any significant apoptotic signals.
Embryos show weak germ band retraction and dorsal closure defects - embryos have a small dorsal hole. Those embryos that fail germ band retraction exhibit apparently normal phase I interaction, however phase II membrane apposition fails completely. Most striking is the failure of the dorsal anterior region of the amnioserosa to initiate contact with the yolk sac membrane, with subsequent high penetrance failure of dorsal closure.
The three longitudinal fascicles, as visible with Fas2, are intact in mys1 mutants. Midline fusions of the most medial tract are seen in some segments.
12/52 neuroblast clones in the mushroom body show obvious overextension of dorsal lobe axons. Both overextension of thin axon bundles near the tip of the dorsal lobe and overextension of a large portion of the dorsal axons is seen.
No anti-βPS staining at muscle attachment sites.
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Statement
Reference
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Statement
Reference
mys1/mys[+] is an enhancer of visible | dominant phenotype of sogEP7
mys1/mys[+] is an enhancer of visible | dominant phenotype of sogEP11
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Statement
Reference
mys1 is a non-enhancer of cell polarity defective phenotype of S05671
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Statement
Reference
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Statement
Reference
mys1 is a non-suppressor of cell polarity defective phenotype of S05671
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Statement
Reference
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Statement
Reference
mys1 has dorsal closure embryo phenotype, enhanceable by BsgNP6293/Bsg[+]
mys1 has embryonic/larval optic stalk phenotype, enhanceable by Fak56DCG1/Fak56D[+]
mys1 has fascicle phenotype, enhanceable by sli2
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Statement
Reference
mys1/mys[+] is an enhancer of embryonic/larval optic stalk phenotype of Fak56DCG1
mys1/mys[+] is an enhancer of heart primordium phenotype of sli2
mys1/mys[+] is an enhancer of oocyte phenotype of Lar5.5/Lar13.2
mys1/mys[+] is an enhancer of wing vein phenotype of sogEP7
mys1/mys[+] is an enhancer of wing vein phenotype of sogEP11
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Statement
Reference
mys1/mys[+] is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoScer\UAS.cUa
mys1 is a non-enhancer of ommatidium phenotype of S05671
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Statement
Reference
hideNOT Suppressor of
Statement
Reference
mys1/mys[+] is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoScer\UAS.cUa
mys1 is a non-suppressor of ommatidium phenotype of S05671
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Statement
Reference
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Statement
Reference
Approximately 24% of mys[1]/+; p130CAS[1]/p130CAS[1] double mutants emerge as adults.
mys[1]/+ ; Df(3L)Exel6083/+ double heterozygotes show axon guidance defects characteristic of increased fasciculation in the ISNb pathway (75.4% of hemisegments), in the SNa pathway (41.8% of hemisegments) and in the central nervous system (40.0% of hemisegments). These defects are not seen in either single heterozygote. The axon guidance defects seen in the ISNb pathway, SNa pathway and central nervous system of embryos expressing p130CAS[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[elav.PLu] are significantly rescued by mys[1]/+.
Fak56DCG1 mys1 double heterozygotes show more severe defects in optic stalk morphology than either single heterozygote, which each show only slight defects in optic stalk formation.
mys1/+; sli2/+ embryos show delayed migration of cardial cells, and clumping of heart cells.
A mys1/+ background does not affect the Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs ommatidial phenotype.
Homozygous mys1 embryos also heterozygous for BsgNP6293 show an enhancement of the dorsal hole phenotype seen in mys1 embryos.
Heterozygous mys1 has no effect on the S05671/+ ommatidial polarity phenotype.
S48-5/mys1 mutants show 7.64%+-3.82 misrotated ommatidia compared to 9.55%+-1.43 seen in S48-5 mutants alone.
The penetrance and expressivity of the germ band retraction defect seen in embryos in which EcRhs.T:Scer\GAL4 is expressed using heat shock for 3 to 5 hours after egg laying is enhanced by mys1/+.
In mys1/+ sli2/+ double heterozygous mutants the frequency of midline guidance errors is increased over the level observed in mys1 homozygous mutants. Apart from midline axon crossings in one-third of the segments, the longitudinal tracts (as visible with Fas2) appear normal.
The addition of mys1/+ to Lar5.5/Lar13.2 increases the penetrance of the oocyte elongation phenotype from 14.1% to about 40%.
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Statement
Reference
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Fails to complement
Comments
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Bloomington
Kyoto
105704
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Discoverer
Poulson Oct. 1948.
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Reported As
Symbol Synonym
l(1)48j
 
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Secondary FlyBase IDs
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hide Recent research papers ( 1 )
Tikhmyanova et al., 2010, PLoS ONE 5(8): e12369
Dcas supports cell polarization and cell-cell adhesion complexes in development. [FBrf0211678]