FB2024_03 , released June 25, 2024
Allele: Dmel\mys11
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General Information
Symbol
Dmel\mys11
Species
D. melanogaster
Name
FlyBase ID
FBal0012688
Feature type
allele
Associated gene
Dmel\mys
Associated Insertion(s)
Carried in Construct
Also Known As
mysXG43, l(1)mysxG43, myospheroidXG43
Key Links
Genomic Maps

Allele class

loss of function allele

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Brown, 1994, Reuter et al., 1993, Bunch et al., 1992)

loss of function allele

(Jannuzi et al., 2002, Roote and Zusman, 1996, Volk et al., 1990, Zusman et al., 1990)
Mutagen
ethyl methanesulfonate
(Zusman et al., 1990, Wilcox et al., 1989)
Progenitor genotype
Cytology
Description

Deletion of nucleotides 2110-2222, resulting in a frame shift after amino acid residue 704.

(Jannuzi et al., 2002)

Approximately 100 bp deletion, between nucleotides 2054 and 2474, in the fourth exon. Faint residual band on immunoblots (as for Df(1)C128) where product is thought to be a remnant from the maternal supply.

(Bunch et al., 1992)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
deletion
X:8,068,418..8,068,530 [+]
Comment:

113 base deletion causes a frameshift after aa residue 704.

(Jannuzi et al., 2002)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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

      abdominal 2 segment border muscle cell

      (Brown, 1994)

      abdominal 3 segment border muscle cell

      (Brown, 1994)

      abdominal 4 segment border muscle cell

      (Brown, 1994)

      abdominal 5 segment border muscle cell

      (Brown, 1994)

      abdominal 6 segment border muscle cell

      (Brown, 1994)

      abdominal 7 segment border muscle cell

      (Brown, 1994)

      adult cardial valve | precursor

      (Pankratz and Hoch, 1995)

      adult cuticle | somatic clone

      (Zusman et al., 1990)

      adult dorsal superficial tracheal branch

      (Stark et al., 1997)

      adult posterior midgut epithelium | somatic clone

      (Lin et al., 2013)

      amnioserosa

      (Narasimha and Brown, 2004, Schock and Perrimon, 2003, Roote and Zusman, 1995)

      anterior midgut primordium | germline clone

      (Martin-Bermudo et al., 1999)

      anterior midgut primordium | maternal effect

      (Devenport and Brown, 2004)

      bouton & neuromuscular junction

      (Beumer et al., 1999)

      bouton & neuromuscular junction & abdominal ventral longitudinal muscle 1

      (Beumer et al., 1999)

      central nervous system

      (Roote and Zusman, 1995)

      circular visceral muscle primordium | maternal effect

      (Devenport and Brown, 2004)

      embryo | dorsal closure stage, with mysD192A.S194A.EYFP.Ubi-p63E

      (Pines et al., 2011)

      embryo | extended germ band stage | germline clone

      (Martin-Bermudo et al., 1999)

      embryonic/first instar larval cuticle | dorsal

      (Li et al., 1998, Grinblat et al., 1994)

      embryonic/larval midgut | embryonic stage

      (Li et al., 1998, Brown, 1994)

      embryonic/larval midgut | embryonic stage | germline clone

      (Martin-Bermudo et al., 1999)

      embryonic/larval proventriculus | embryonic stage

      (Brown, 1994)

      embryonic/larval salivary gland | embryonic stage

      (Stark et al., 1997)

      embryonic/larval somatic muscle cell

      (Loer et al., 2008, Li et al., 1998, Brown, 1994, Grinblat et al., 1994)

      embryonic/larval visceral muscle & midgut

      (Devenport and Brown, 2004)

      embryonic/larval visceral tracheal branch

      (Boube et al., 2001)

      embryonic dorsal epidermis

      (Brown, 1994)

      embryonic epidermis | dorsal

      (Zusman et al., 1993)

      embryonic midgut constriction

      (Devenport and Brown, 2004, Roote and Zusman, 1995, Brown, 1994)

      embryonic somatic muscle cell

      (Jani and Schock, 2007)

      eye

      (Grinblat et al., 1994)

      eye | somatic clone

      (Zusman et al., 1993)

      female germline cyst | somatic clone

      (Bolivar et al., 2006)

      filamentous actin | somatic clone

      (Delon and Brown, 2009)

      follicle cell | somatic clone

      (Delon and Brown, 2009, Bolivar et al., 2006)

      gastric caecum

      (Brown, 1994)

      germ band

      (Schock and Perrimon, 2003)

      germ band, with mysD192A.S194A.EYFP.Ubi-p63E

      (Pines et al., 2011)

      germ band, with mysS196F.EYFP.Ubi-p63E

      (Pines et al., 2011)

      germ layer | embryonic stage

      (Li et al., 1998)

      haltere | somatic clone

      (Zusman et al., 1990)

      larval ventral nerve cord

      (Brown, 1994)

      leg | somatic clone

      (Zusman et al., 1990)

      midgut primordium

      (Li et al., 1998)

      mitotic domain 1 | extended germ band stage

      (Roote and Zusman, 1995)

      muscle attachment site

      (Prokop et al., 1998)

      muscle cell of abdominal 2 lateral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 2 ventral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 3 lateral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 3 ventral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 4 lateral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 4 ventral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 5 lateral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 5 ventral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 6 lateral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 6 ventral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 7 lateral longitudinal muscle 1

      (Brown, 1994)

      muscle cell of abdominal 7 ventral longitudinal muscle 1

      (Brown, 1994)

      muscle tendon junction, with mys804stop.EYFP.Ubi-p63E

      (Pines et al., 2011)

      muscle tendon junction, with mysD192A.S194A.EYFP.Ubi-p63E

      (Pines et al., 2011)

      muscle tendon junction, with mysD807R.EYFP.Ubi-p63E

      (Pines et al., 2011)

      muscle tendon junction, with mysS196F.EYFP.Ubi-p63E

      (Pines et al., 2011)

      neuromuscular junction

      (Beumer et al., 1999)

      neuromuscular junction (with mysolfC-x17)

      (Beumer et al., 2002)

      neuromuscular junction & abdominal lateral longitudinal muscle 1

      (Beumer et al., 1999)

      ommatidium | somatic clone

      (Zusman et al., 1990)

      pericardial cell

      (Stark et al., 1997)

      posterior midgut primordium | germline clone

      (Martin-Bermudo et al., 1999)

      presumptive embryonic salivary gland | maternal effect

      (Bradley et al., 2003)

      rhabdomere | somatic clone

      (Zusman et al., 1990)

      salivary gland common duct primordium

      (Roote and Zusman, 1995)

      salivary gland common duct primordium | germline clone

      (Martin-Bermudo et al., 1999)

      salivary gland common duct primordium | maternal effect

      (Devenport and Brown, 2004)

      somatic muscle cell

      (Roote and Zusman, 1995)

      stalk follicle cell | somatic clone

      (Bolivar et al., 2006)

      stress fiber | somatic clone

      (Delon and Brown, 2009)

      tendon cell | embryonic stage

      (Martin-Bermudo, 2000)

      tergite | somatic clone

      (Zusman et al., 1990)

      terminal tracheal cell | somatic clone

      (Levi et al., 2006)

      tracheal dorsal trunk primordium

      (Boube et al., 2001)

      visceral mesoderm

      (Roote and Zusman, 1995)

      visceral mesoderm | germline clone

      (Martin-Bermudo et al., 1999)

      wing

      (Grinblat et al., 1994)

      wing | somatic clone

      (Zusman et al., 1993, Zusman et al., 1990)

      wing blade | somatic clone

      (Bokel et al., 2005)

      wing vein | somatic clone

      (Zusman et al., 1990)

      Z disc

      (Volk et al., 1990)
      Detailed Description
      Statement
      Reference

      Adult-generated mys11 homozygous mutant intestinal stem cell clones have reduced maintenance 7 days and 14 days after clone induction compared to control clones; remaining clones contain fewer cells by day 14 and many only contain differentiated cells; enteroendocrine cell/enterocyte ratio is unaffected and intestinal stem cells show no obvious signs of apoptosis.

      (Lin et al., 2013)

      mys11 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.

      (Nagaosa et al., 2011)

      Approximately 47% of mys11 mutant embryos, lacking both maternal and zygotic mys, fail to undergo germband retraction, while approximately 67% fail to complete dorsal closure.

      mys11 mutant embryos exhibit a muscle detachment phenotype at stage 17, characteristic of a myotendinous junction failure at stage 16.

      (Pines et al., 2011)

      mys11 follicle cell clones form stress fibres (prominent bundles of F-actin on their basal surface) similar to wild type. However, these bundles are not organized into the normal parallel arrangement and are displaced towards the periphery. Follicle cell shape is changed - they are no longer hexagonal and are unable to flatten fully. mys11 follicle cell clones also show F-actin aggregates.

      (Delon and Brown, 2009)

      Homozygous embryos show a detached muscle phenotype.

      (Loer et al., 2008)

      mys11 zygotic mutant embryos show a detached muscle phenotype.

      (Jani and Schock, 2007)

      Homozygous clones induced throughout the somatic cells of the germarium results in the absence of interfollicular stalks between egg chambers, cysts containing less than 16 cells, failed follicle cell migration and an abnormal orientation of cysts along the anterior-posterior axis.

      Homozygous clones induced in the follicle cells but not the escort cells of the female germarium do not show abnormal alignment of cysts.

      (Bolivar et al., 2006)

      Zygotic mys11 embryos do not show a phenotype in macrophage shape or migration.

      (Huelsmann et al., 2006)

      mys11 dorsal branch terminal cell clones in third instar larvae show substantial branch pruning and multiple convoluted lumens coursing through the remaining terminal branches. When individual mys11 clones are imaged in live early third instar larvae and again 48 hours later, terminal branches are lost or collapsed as the multi-lumen defect becomes more prominent. Lumens are often displaced from branches before the branch is completely lost.

      (Levi et al., 2006)

      Clones of mutant cells in the pupal wing still contain the transalar microtubule arrays that are normally seen spanning the wing cells at this stage. The bundles are disordered in the mutant cells, presumably because of the separation between the two cell layers of the wing that is seen in wings carrying mutant clones.

      (Bokel et al., 2005)

      In mys11 homozygotes the midgut forms primary constrictions but these fail to elongate, resulting in a poorly convoluted midgut by stage 17. This may be a secondary effect of defects in the visceral muscle surrounding the midgut, as this fails to flatten in stage 16 embryos. In embryos maternally & zygotically homozygous for mys11, migration of the midgut primordia is delayed and the visceral mesoderm along which these primordia migrate (circular visceral muscle primordium?) is somewhat disorganized.

      (Devenport and Brown, 2004)

      Mutant embryos exhibit four defects in cellular organisation: detachment between the amnioserosa and the yolk cell; failure in the elongation of amnioserosa cells along the apical-basal axis; apical expansion of the amnioserosa cells at the interface and the loss of the normally extended contact with the leading edge; and loss of adhesion between amnioserosa cells and, at the amnioserosa leading edge interface.

      (Narasimha and Brown, 2004)

      Homozygous embryos (lacking zygotic mys function) do not have defects in salivary gland migration, whereas embryos lacking both maternal and zygotic mys function have abnormally shaped and positioned salivary glands.

      (Bradley et al., 2003)

      65% of mys11 maternal and zygotic mutants exhibit a u-shaped embryo phenotype which results from a failure of germ-band retraction. These embryos exhibit pleiotropic defects most evident in the amnioserosa. The overlap of the amnioserosa over the tail end of germ band is defective, whereas cell-shape changes in the amnioserosa epithelium frequently exhibit multilayering, suggesting polarity defects.

      (Schock and Perrimon, 2003)

      mysolfC-x17/mys11 synapses at the larval neuromuscular junction show overgrowth.

      (Beumer et al., 2002)

      Mutant embryos show dorsal herniation.

      (Jannuzi et al., 2002)

      In mutant embryos, the visceral branches of the tracheal system are shorter than wild-type, though fine branches still exist. During development, they reach and contact the visceral mesoderm, but do not migrate along the mesoderm. In addition, visceral branches sometimes detach from the visceral mesoderm, some mutant embryos show gaps in the dorsal trunk and defects in the dorsal branch.

      (Boube et al., 2001)

      The tendon matrix appears disorganised in homozygous embryos derived from homozygous females and the muscles detach.

      (Martin-Bermudo, 2000)

      The neuromuscular junctions of mysb9/mys11 larvae contain small, tightly clustered boutons surrounded by numerous mini-boutons. The neuromuscular junctions of mysts1/mys11 larvae show no significant increase in bouton numbers. mysb9/mys11 larvae show altered synapse specificity at the muscle 12 NMJ. More than 30% of NMJs show a "backbranched" phenotype; at least one arboreal branch leaves muscle 12 and branches back onto muscle 13 from a site away from the point of nerve entry onto muscle 12. 50% of mysb9/mys11 muscle 12 NMJs show a "pulled away" phenotype; boutons are suspended in the space between muscles 12 and 13 and defasciculation, or branching, occurs before the nerve has actually reached the point of insertion on the muscle. mysts1/mys11 larvae show altered synapse specificity at the muscle 12 NMJ. The NMJs may show a "backbranched" phenotype; at least one arboreal branch leaves muscle 12 and branches back onto muscle 13 from a site away from the point of nerve entry onto muscle 12. The NMJs may show a "pulled away" phenotype; boutons are suspended in the space between muscles 12 and 13 and defasciculation, or branching, occurs before the nerve has actually reached the point of insertion on the muscle. The NMJs may show a "multiple insertions" phenotype, where two or more separate and distinct nerve entry points can be seen on muscle 12. In these junctions, both nerves can frequently be traced back to a point of separation above muscle 13. SSR morphology appears qualitatively unaffected in type I NMJs of mysb9/mys11 larvae and the SSR mean cross-section area is not significantly different from wild type. Boutons appear ultrastructurally normal and the presynaptic membranes are normally attached to the postsynaptic membrane. Synaptic vesicle density is indistinguishable from wild type. At the muscle 4 and 6 NMJs, nerve-evoked excitatory junctional current (EJC) amplitudes appear normal in mysb9/mys11 larvae. mysts1/mys11 larvae have significantly larger nerve-evoked excitatory junctional current (EJC) amplitudes than normal at the muscle 4 NMJ.

      (Beumer et al., 1999)

      The endodermal midgut cells remain rounded, do not have projections and are delayed in their migration in embryos lacking both maternal and zygotic mys function (derived from homozygous female germline clones). The anterior midgut primordium and posterior midgut primordium do eventually meet in these embryos, but not until stage 15, and therefore migration is delayed by approximately 2 hours. Interruptions and irregularities are seen in the visceral mesoderm in these embryos. Defects in the retraction of the germband are also seen.

      (Martin-Bermudo et al., 1999)

      Attachment of muscles to the epidermis is disturbed in stage 16 homozygous embryos.

      (Prokop et al., 1998)

      Pericardial cells appear to dissociate, migrate randomly and are sparse. Embryos exhibit significant gaps in the dorsal trunk of the trachea. Embryos frequently display one salivary gland misshapen and smaller than the other, the gland may also be shifted closer to the midline.

      (Stark et al., 1997)

      cnomis1 homozygotes that are heterozygous with mys11 exhibit extra wing vein material.

      (Miyamoto et al., 1995)

      Cardiac arrest phenotype, foregut cells are clustered at the top of the proventriculus and cannot migrate inside to form the cardiac valve.

      (Pankratz and Hoch, 1995)

      Embryos lacking both maternal and zygotic mys expression show extension of the germband laterally rather than dorsally. Mutant embryos show a distinct and reproducible separation between the ectodermal and mesodermal tissue layers of the germband, though the separation is not complete. Dorsal closure proceeds but is followed by dorsal rupture and the posterior tissue moving dorsally and anteriorly producing a tail-up phenotype. Subtle abnormalities are evident during germ band retraction. The amnioserosa detaches from the end of the hindgut. At the end of germband retraction the anterior ventral cells of the germband move slightly more anteriorly than corresponding tissue in wild type animals. Anterior and posterior midgut primordia are abnormally shaped by late germband extension. Invagination is normal but the cells remain as spherical masses. This phenotype is only observed if the embryos lack both maternal and zygotic mys product. Mutant embryos show interruptions and irregularities in the visceral mesoderm. Midgut constrictions in stage 16 embryos are at best barely visible. Embryos missing only zygotic expression have near normal midgut constrictions. Somatic muscles detach, a hole is evident in the dorsal cuticle and the nervous system shows incomplete condensation.

      (Roote and Zusman, 1995)

      Midgut constrictions do not fully form. Midgut and gastric caecae do not elongate and by the end of stage 16 the proventriculus is also abnormal. Many somatic muscles have detached and rounded up by the middle of stage 16. Ventral nerve cord only partly contracts. The supraoesophageal ganglia and presumptive optic lobes become distorted in mys embryos because they are pushed through the dorsal hole. Dorsal closure occurs normally, but shortly after the edges of the epidermis separate, resulting in a dorsal hole. Later morphogenetic movements promote a secondary dorsal closure, resulting in a grooved appearance of the epidermis surrounding the hole, and the constriction of internal tissues.

      (Brown, 1994)

      Embryos die with a dorsal hole in the cuticle. In clones, blisters form in the wing, and ommatidia are disorganized.

      (Grinblat et al., 1994)

      Homozygous clones in the wing result in wing blisters. In clones in the eye this allele causes a disorganised photoreceptor phenotype, although there is the normal number of photoreceptors per ommatidium. Mutant embryos have a dorsal hole.

      (Zusman et al., 1993)

      No anti-βPS staining at muscle attachment sites.

      (Bunch et al., 1992)

      Characteristic membranal localisation MSP-300, and concentration at attachment sites is not prominent in mys11.

      (Volk, 1992)

      Cells derived from homozygous late gastrula embryos appear less stretched out and more rounded and have fewer cell-cell contacts than wild-type cells when cultured in vitro on laminin-coated coverslips. Muscles of homozygous embryos lack defined Z bands. Multinucleate myotubes are seen in these embryos.

      (Volk et al., 1990)

      In adults mosaic for mys function, mutant patches were small and covered no more than 10% of the fly. Wing blisters, missing legs or leg parts, tergite defects and missing pieces of cuticle were frequently observed. Folds in one or both surfaces of the wing, vein abnormalities and missing or enlarged halteres were also seen. The largest mutant patches were in the dorsally located tergites, and could be normal or defective in appearance. The structure of the rhabdomeres in mys mutant ommatidia was abnormal. There is a strong bias for lethality in those mosaics that have mutant cells in ventrally derived structures.

      (Zusman et al., 1990)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Enhanced by
      Statement
      Reference

      mys11 has adult posterior midgut epithelium | somatic clone phenotype, enhanceable by Scer\GAL4Act.PU/ItgbnGD7

      (Lin et al., 2013)

      mys11 has embryonic/larval optic stalk phenotype, enhanceable by FakCG1/Fak56D[+]

      (Murakami et al., 2007)

      mys11 has anterior midgut primordium phenotype, enhanceable by Itgbn1/Itgbn1

      (Devenport and Brown, 2004)

      mys11 has embryonic/larval visceral muscle & midgut phenotype, enhanceable by Itgbn1/Itgbn1

      (Devenport and Brown, 2004)

      mys11 has embryonic midgut constriction phenotype, enhanceable by Itgbn1/Itgbn1

      (Devenport and Brown, 2004)

      mys11 has salivary gland common duct primordium | maternal effect phenotype, enhanceable by Itgbn1

      (Devenport and Brown, 2004)
      NOT Enhanced by
      Statement
      Reference

      mys11 has circular visceral muscle primordium | maternal effect phenotype, non-enhanceable by Itgbn1/Itgbn1

      (Devenport and Brown, 2004)

      mys11/mys8 has wing phenotype, non-enhanceable by pot[+]/potP3

      (Walsh and Brown, 1998)
      Suppressed by
      Statement
      Reference

      mys11 has adult posterior midgut epithelium | somatic clone phenotype, suppressible by Scer\GAL4Act.PU/ItgbnUAS.cUa

      (Lin et al., 2013)

      mys11 has phenotype, suppressible by vnUAS.cYa/Scer\GAL469B

      (Martin-Bermudo, 2000)
      NOT suppressed by
      Enhancer of
      Statement
      Reference

      mys11/mys[+] is an enhancer of embryonic/larval optic stalk phenotype of FakCG1

      (Murakami et al., 2007)

      mys11/mys[+] is an enhancer of mitotic domain 1 | extended germ band stage phenotype of EcRGAL4::LBD.hs

      (Kozlova and Thummel, 2003)
      Suppressor of
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      mys11 homozygous embryos expressing VincCO.Scer\UAS.P\T.T:Equa\eqFP578-TagRFP under the control of Scer\GAL4Mef2.PU present severe muscle defects, including detachment and rounding-up of muscles, as compared to controls; mys homozygosity also leads to a moderate reduction in the number of ectopic VincCO.Scer\UAS.P\T.T:Equa\eqFP578-TagRFP-positive cytoplasmic protein aggregates formed upon Scer\GAL4Act5C.PU-driven expression in follicle cell clones.

      (Maartens et al., 2016)

      Fak56DCG1 mys11 double heterozygotes show more severe defects in optic stalk morphology than either single heterozygote, which each show only slight defects in optic stalk formation.

      (Murakami et al., 2007)

      The macrophage phenotype of Scer\GAL4srp>Gef26EP388 embryos is suppressed by a mys11 background; these macrophages have the appearance of wild-type cells regarding size and protrusions.

      The macrophage phenotype of Scer\GAL4srp>RV12.Scer\UAS.T:Hsap\MYC embryos is suppressed in a mys11 background; these macrophages show no enlargement of protrusions, or cell shape change.

      (Huelsmann et al., 2006)

      Homozygous mys11 follicle cell or germ-line clones that are induced in homozygous βInt-νunspecified females do not result in oocyte mislocalisation.

      (Becam et al., 2005)

      Midgut constrictions fail to form in mys11; βInt-ν1 double homozygotes. This may be a secondary effect of defects in the visceral muscle surrounding the midgut: the midgut is initially enclosed by visceral muscle, but by stage 16 this muscle becomes highly disorganized and patchy and detaches from the underlying endoderm. (Note these phenotypes are for embryos maternally and zygotically βInt-ν1/βInt-ν1 - zygotic alone not tested). In embryos maternally and zygotically homozygous for mys11 and βInt-ν1, migration of the midgut primordia fails to occur. However, disorganization of the visceral mesoderm (circular visceral muscle primordium?) seen in mys11 maternal/zygotic homozygotes in not enhanced. Other mutant phenotypes of mys11 mutant embryos (defects in dorsal closure, germ-band retraction and muscle detachement) are unaffected by βInt-ν1. The delay in migration of the midgut primordia in embryos maternally & zygotically homozygous for mys11 is not suppressed by βInt-νEP2235; Scer\GAL448Y. When border cells are part of a mys11/mys11 somatic clone in a βInt-ν1/βInt-ν2 background, border cell migration occurs normally. βInt-ν1/βInt-ν2 also has no obvious effect on the phenotypes or size of somtic clones in the columnar follicle cell or in the imaginal discs.

      (Devenport and Brown, 2004)

      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 mys11/+.

      (Kozlova and Thummel, 2003)

      Expression of vnScer\UAS.cYa in the tendon cells under the control of Scer\GAL469B can rescue the phenotype of mys11 embryos (that lack both maternal and zygotic mys function), while expression of vnScer\UAS.cYa in the mesoderm under the control of both Scer\GAL4twi.PG and Scer\GAL4how-24B cannot.

      (Martin-Bermudo, 2000)

      The frequency of wing blisters seen in mys11/mys8 flies is not dominantly enhanced by potP3.

      (Walsh and Brown, 1998)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Complements

      mysts3

      (Bunch et al., 1992)

      mysts2

      (Bunch et al., 1992)
      Fails to complement

      mysts1

      (Bunch et al., 1992)
      Rescued by

      mys11/mysG1 is rescued by mysUbi-p63E.Venus

      (Ellis et al., 2011)

      mys11 is rescued by mysL211I.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is rescued by mysG792N.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is rescued by mysD807R.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is rescued by mysY831F.Y843F.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is rescued by mysUbi-p63E.Venus

      (Pines et al., 2011)

      mys11 is rescued by Scer\GAL4Kr.PM/mysdin.UAS

      (Schock and Perrimon, 2003)

      mys11 is rescued by mystZa

      (Li et al., 1998)

      mys11 is rescued by mysrYYF

      (Li et al., 1998)

      mys11 is rescued by mysrDEA

      (Grinblat et al., 1994)

      mys11 is rescued by mysrYYF

      (Grinblat et al., 1994)

      mys11 is rescued by mysdin

      (Grinblat et al., 1994)
      Partially rescued by

      mys11 is partially rescued by Scer\GAL4Act.PU/mysUAS.cLa

      (Lin et al., 2013)

      mys11/mysG1 is partially rescued by mysE810Q.E817Q.Ubi-p63E.Venus

      (Ellis et al., 2011)

      mys11 is partially rescued by mysD192A.S194A.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is partially rescued by mysL796R.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is partially rescued by mys804stop.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is partially rescued by mysN840A.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is partially rescued by mysdin.UAS/Scer\GAL448Y

      (Martin-Bermudo et al., 1999)

      mys11 is partially rescued by Scer\GAL4twi.PG/Scer\GAL4how-24B/mysdin.UAS

      (Martin-Bermudo et al., 1999)

      mys11 is partially rescued by mysrFFA

      (Li et al., 1998)

      mys11 is partially rescued by mysrDEA

      (Li et al., 1998)

      mys11 is partially rescued by mysrFFA

      (Grinblat et al., 1994)

      mys11 is partially rescued by mystZa

      (Grinblat et al., 1994)

      mys11 is partially rescued by mys4B

      (Zusman et al., 1993)

      mys11 is partially rescued by mys4B.hs

      (Zusman et al., 1993)

      mys11 is partially rescued by mystZa

      (Zusman et al., 1993)

      mys11 is partially rescued by mys4A

      (Zusman et al., 1993)

      mys11 is partially rescued by mys4A.hs

      (Zusman et al., 1993)
      Not rescued by

      mys11/mysG1 is not rescued by mysN828A.Ubi-p63E.Venus

      (Ellis et al., 2011)

      mys11 is not rescued by mysS196F.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is not rescued by mysD807R.EYFP.Ubi-p63E

      (Pines et al., 2011)

      mys11 is not rescued by myst2

      (Li et al., 1998)

      mys11 is not rescued by myst1

      (Li et al., 1998)

      mys11 is not rescued by myst2

      (Grinblat et al., 1994)

      mys11 is not rescued by myst1

      (Grinblat et al., 1994)
      Comments

      mysE810Q.E817Q.Ubi-p63E.T:Avic\GFP-YFP.Venus fails to rescue the germband retraction and dorsal closure defects of mys11/mysG1 embryos, but partially rescues the myotendinous junction defects.

      (Ellis et al., 2011)

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

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

      Expression of mysUbi-p63E.T:Avic\GFP-EYFP 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.

      (Pines et al., 2011)

      The ability of the endodermal midgut cells of embryos that lack maternal and zygotic mys function (derived from homozygous mys11 female germline clones) to send projections and to migrate is rescued by mysdin.Scer\UAS expressed under the control of Scer\GAL448Y, although there is a small delay in migration. The visceral mesoderm and germband retraction defects are not rescued in these embryos. mysdin.Scer\UAS expressed under the control of both Scer\GAL4twi.PG and Scer\GAL4how-24B rescues the visceral mesoderm defects of embryos that lack maternal and zygotic mys function (derived from homozygous mys11 female germline clones) but does not rescue the migration defects of the endodermal midgut cells in these embryos.

      (Martin-Bermudo et al., 1999)

      Expression of mystZa or mysrYYF rescues embryonic abnormalities of mutants. Many embryonic abnormalities are not rescued by myst1 (the attachment of the germ layers of the embryonic germband and the initial formation of midgut constrictions are rescued). Germband separation and midgut constrictions of mys11 embryos are rescued by expression of mysrDEA or mysrFFA. mysrDEA also rescues defects in midgut migration and elongation and in maintaining closure of the embryonic cuticle.

      (Li et al., 1998)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      Comments
      Comments

      No PSβ protein.

      (Wilcox et al., 1989)

      Endoderm migrates normally over the visceral mesoderm.

      (Reuter et al., 1993)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (9)
      Reported As
      Symbol Synonym
      l(1)mysXG43
      (Volk et al., 1990, Zusman et al., 1990)
      l(1)mysxG43
      (Reuter et al., 1993, Wilcox et al., 1989)
      myospheroidXG43
      (Levi et al., 2006, Narasimha and Brown, 2004, Narasimha and Brown, 2004)
      mys11
      (Hunter et al., 2020, Clark et al., 2011, Bolivar et al., 2006)
      mysXG43
      (Santa-Cruz Mateos et al., 2020, Richier et al., 2018, Maartens et al., 2016, Kondo and Hayashi, 2013, Lin et al., 2013, Koper et al., 2012, Ellis et al., 2011, Nagaosa et al., 2011, Pines et al., 2011, Zervas et al., 2011, Bahri et al., 2010, Haghayeghi et al., 2010, Delon and Brown, 2009, Rushton et al., 2009, Loer et al., 2008, Loer et al., 2008, Devenport et al., 2007, Inoue and Hayashi, 2007, Jani and Schock, 2007, Murakami et al., 2007, Subramanian et al., 2007, Volohonsky et al., 2007, Bolivar et al., 2006, Huelsmann et al., 2006, Tanentzapf et al., 2006, Wahlstrom et al., 2006, Becam et al., 2005, Bokel et al., 2005, Devenport and Brown, 2004, Torgler et al., 2004, Bradley et al., 2003, Clark et al., 2003, Kozlova and Thummel, 2003, Schock and Perrimon, 2003, Brown et al., 2002, Jannuzi et al., 2002, Billuart et al., 2001, Boube et al., 2001, Zervas et al., 2001, Martin-Bermudo, 2000, Martin-Bermudo and Brown, 2000, Beumer et al., 1999, Martin-Bermudo and Brown, 1999, Martin-Bermudo et al., 1999, Li et al., 1998, Prokop et al., 1998, Walsh and Brown, 1998, Stark et al., 1997, Hoch and Pankratz, 1996, Martin-Bermudo and Brown, 1996, Roote and Zusman, 1996, Longley and Ready, 1995, Miyamoto et al., 1995, Pankratz and Hoch, 1995, Roote and Zusman, 1995, Brown, 1994, Fogerty et al., 1994, Grinblat et al., 1994, Brown et al., 1993, Zusman et al., 1993, Bunch et al., 1992)
      mysxG43
      (Lovegrove et al., 2019, Volk, 1992)
      mysxg43
      (Beumer et al., 2002)
      mysXG43
      (Sun and Stathopoulos, 2018)
      βPS integrin-
      (Narasimha and Brown, 2004)
      Name Synonyms
      Secondary FlyBase IDs
        References (76)