Open Close
General Information
Symbol
Dmel\mys1
Species
D. melanogaster
Name
FlyBase ID
FBal0012678
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology

Polytene chromosomes normal.

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.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

mys1 homozygous embryos exhibit defects in gonad niche morphogenesis compared to controls.

mys1 mutant class IV da neurons (generated using the MARCM system under the control of Scer\GAL4109(2)80) show a significant increase in the amount of dendrites that cross other dendrites when analysed in a 2D plane. When these crossing overs are examined in ddaC dendrites in the apical-basal plane 88.14% are enclosed in the epidermis rather than attaching to the ECM. These dendrites are thus in different apical-basal planes and are non-contacting.

Homozygous embryos have blisters and gaps in the rows of cardioblasts in the heart region of the dorsal vessel which normally align along the midline. The leading edge membrane of migrating mutant cardioblasts shows less vigorous activity than that of wild-type cardioblasts.

mys1 mutant embryonic hemocytes do not show significant changes in the competence to undertake phagocytosis of apoptotic cells, changes in proportions of hemocytes or apoptotic cells , as compared to controls.

Normal transverse tubule formation is seen in the abdominal temporary eclosion muscles of mys1/mysts1 pharate adults.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference

mys1/mys[+] is an enhancer of visible | dominant phenotype of sogEP7

mys1/mys[+] is an enhancer of visible | dominant phenotype of sogEP11

NOT Enhancer of
Statement
Reference

mys1/mys[+] is a non-enhancer of visible | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU

mys1 is a non-enhancer of abnormal cell polarity phenotype of S05671

Suppressor of
NOT Suppressor of
Statement
Reference

mys1/mys[+] is a non-suppressor of visible | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU

mys1 is a non-suppressor of abnormal cell polarity phenotype of S05671

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

mys1 has embryonic/larval optic stalk phenotype, enhanceable by FakCG1/Fak56D[+]

mys1 has embryo | dorsal closure stage phenotype, enhanceable by BsgNP6293/Bsg[+]

mys1 has fascicle phenotype, enhanceable by sli2

Enhancer of
Statement
Reference

mys1/mys[+] is an enhancer of embryonic/larval optic stalk phenotype of FakCG1

mys1/mys[+] is an enhancer of heart primordium phenotype of sli2

mys1/mys[+] is an enhancer of wing vein phenotype of sogEP7

mys1/mys[+] is an enhancer of wing vein phenotype of sogEP11

mys1/mys[+] is an enhancer of oocyte phenotype of Lar5.5/Lar13.2

NOT Enhancer of
Statement
Reference

mys1/mys[+] is a non-enhancer of wing blade posterior compartment | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU

mys1/mys[+] is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

mys1 is a non-enhancer of ommatidium phenotype of S05671

Suppressor of
NOT Suppressor of
Statement
Reference

mys1/mys[+] is a non-suppressor of wing blade posterior compartment | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU

mys1/mys[+] is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

mys1 is a non-suppressor of ommatidium phenotype of S05671

Other
Additional Comments
Genetic Interactions
Statement
Reference

RetC168 mys1 transheterozygous third instar larvae exhibit defects in class IV dendritic arborizing neuron dendrite crossing and a substantial loss of dendrite-ECM interaction. No phenotypes are observed in either heterozygote alone.

mys1 Rac1J11 transheterozygous third instar larvae exhibit defects in class IV dendritic arborizing neuron dendrite-ECM interaction. The phenotype is not observed in either heterozygote alone.

The wing blistering phenotype seen in the posterior compartment of wings in flies expressing EogtGD5084 under the control of Scer\GAL4en.PU in the presence of Dcr-2Scer\UAS.cDa is not affected if the flies are also heterozygous for mys1.

A mys1/Y background increases the percentage of embryonic segments displaying eg-positive axon midline crossing defects in flies expressing fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360. However, this increase isn't considered statistically significant.

22.62% of mewM6/mys1 mutant class IV da dendrites (generated using the MARCM system under the control of Scer\GAL4109(2)80) are enclosed in the epidermis rather than attached to the ECM. This compares to 4.09% and 4.18% in mys1/+ and mewM6/+ respectively.

mewM6/wb09437 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendrite length that is enclosed within the epidermis rather than attached to the ECM. The amount of enclosed dendrite seen in each heterozygote is similar to wild type.

mys1/LanA9-32 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendritic length that is enclosed within the epidermis rather than attached to the ECM The amount of enclosed dendrite seen in each heterozygote is similar to wild type.

mys1/LanB2MB04039 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendritic length that is enclosed within the epidermis rather than attached to the ECM. The amount of enclosed dendrite seen in each heterozygote is similar to wild type.

mys1/+ ; scb2/+ double heterozygous embryos show defects in continuity and alignment of the cardioblasts at the dorsal midline.

Expression of one copy of Sema-1aScer\UAS.cYa under the control of Scer\GAL4how-24B in embryos that are also heterozygous for mys1 results in axon guidance defects in the ISNb and SNa nerves, resulting in reduced muscle innervation.

Approximately 24% of mys1/+; p130CAS1/p130CAS1 double mutants emerge as adults.

No significant overgrowth of the neuromuscular junction is seen in FakN30/FakKG00304 third instar larvae which are also heterozygous for mys1.

mys1/+ ; 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 p130CASScer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PLu are significantly rescued by mys1/+.

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%.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Approximately 5% of mys11 mutant embryos expressing mysUbi-p63E.T:Avic\GFP-YFP.Venus fail to undergo germband retraction, indicating rescue.

Expression of mysUbi-p63E.T:Avic\GFP-YFP.Venus rescues the dorsal closure defects seen in mys11 mutant embryos.

Expression of mysUbi-p63E.T:Avic\GFP-YFP.Venus rescues the myotendinous junction failure seen in mys11 embryos.

Expression of mysD19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E partially rescues the germband retraction phenotype found in mys11 embryos. However, the dorsal closure defects found in these embryos was not rescued and indeed in many cases appeared more severe.

The mysD19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E transgene confers a 22.5% rescue of myotendinous junction failure (leading to muscle attachment defects) in mid- to late-stage 17 embryos, however myotendinous junction failure is fully penetrant by early larval stages. This indicates that muscle attachment is delayed in embryos rescued with mysD19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E.

Expression of mysS196F.T:Avic\GFP-EYFP.Ubi-p63E fails to rescue both the germband retraction and dorsal closure phenotypes found in mys11 embryos.

The mysS196F.T:Avic\GFP-EYFP.Ubi-p63E transgene fails to rescue the muscle detachment phenotype seen in mys11 embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type.

Expression of mysL211I.T:Avic\GFP-EYFP.Ubi-p63E rescues both the germband retraction and dorsal closure phenotypes found in mys11 embryos.

The mysL211I.T:Avic\GFP-EYFP.Ubi-p63E transgene rescues the muscle detachment phenotype seen in mys11 embryos.

Expression of mysG792N.T:Avic\GFP-EYFP.Ubi-p63E rescues both the germband retraction and dorsal closure phenotypes found in mys11 embryos.

The mysG792N.T:Avic\GFP-EYFP.Ubi-p63E transgene rescues the muscle detachment phenotype seen in mys11 embryos.

Expression of mysL796N.T:Avic\GFP-EYFP.Ubi-p63E partially rescues the germband retraction phenotype and almost completely rescues the dorsal closure phenotype found in mys11 embryos.

The mysL796N.T:Avic\GFP-EYFP.Ubi-p63E transgene rescues the muscle detachment phenotype seen in mys11 embryos.

Expression of mys804stop.T:Avic\GFP-EYFP.Ubi-p63E partially rescues the germband retraction phenotype and fails to rescue the dorsal closure phenotype found in mys11 embryos. Indeed in many cases the dorsal closure defects appear more severe.

The mys804stop.T:Avic\GFP-EYFP.Ubi-p63E transgene fails to rescue the muscle detachment phenotype seen in mys11 embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type.

Expression of mysD807R.T:Avic\GFP-EYFP.Ubi-p63E rescues both the germband retraction and dorsal closure phenotypes found in mys11 embryos.

The mysD807R.T:Avic\GFP-EYFP.Ubi-p63E transgene fails to rescue the muscle detachment phenotype seen in mys11 embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type.

Expression of mysY831F.Y843F.T:Avic\GFP-EYFP.Ubi-p63E rescues the germband retraction phenotype but exacerbates the dorsal closure phenotype found in mys11 embryos.

The mysY831F.Y843F.T:Avic\GFP-EYFP.Ubi-p63E transgene rescues the muscle detachment phenotype seen in mys11 embryos.

Expression of mysN840A.T:Avic\GFP-EYFP.Ubi-p63E partially rescues both the germband retraction and dorsal closure phenotypes found in mys11 embryos.

The mysN840A.T:Avic\GFP-EYFP.Ubi-p63E transgene partially rescues the muscle detachment phenotype seen in mys11 embryos. Although myotendinous junction length appears fully rescued in these animals, there is a mild but significant reduction in myotendinous area compared to wild-type.

Images (0)
Mutant
Wild-type
Stocks (3)
Notes on Origin
Discoverer

Poulson Oct. 1948.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (49)