Allele Dmel\mys¹¹

General Information
Symbol	Dmel\mys¹¹	Species	D. melanogaster
Name		FlyBase ID	FBal0012688
Feature type	allele	Associated gene	Dmel\mys
Also Known As	mys^XG43, l(1)mys^xG43, myospheroid^XG43

Map ( GBrowse )
Allele class	amorphic allele - genetic evidence, loss of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02	Controlled Vocabulary Terms dorsal closure stage embryo muscle tendon junction
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	amorphic allele - genetic evidence (Bunch et al., 1992, Reuter et al., 1993, Brown, 1994) loss of function allele (Volk et al., 1990, Zusman et al., 1990, Roote and Zusman, 1996, Jannuzi et al., 2002)
Mutagen	ethyl methanesulfonate (Wilcox et al., 1989, Zusman et al., 1990)
Mutations Mapped to the Genome

Type Location Additional Notes References deletion X:7,962,451..7,962,563 evidence=experimental comment=113 base deletion causes a frameshift after aa residue 704. (Jannuzi et al., 2002)
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 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)
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| embryonic stage (Bunch et al., 1992, Zusman et al., 1990) lethal \| embryonic stage \| recessive (Zusman et al., 1993) lethal \| recessive (Grinblat et al., 1994) neuroanatomy defective (with mys^olfC-x17) (Beumer et al., 2002) neuroanatomy defective \| larval stage (with mys^b9) (Beumer et al., 1999) neuroanatomy defective \| larval stage (with mys^ts1) (Beumer et al., 1999) neurophysiology defective \| larval stage (with mys^ts1) (Beumer et al., 1999) visible \| dorsal closure stage, with mys^{S196F.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) visible \| dorsal closure stage (with mys^{Ubi-p63E.T:Avic\GFP-EYFP}) (Pines et al., 2011) visible \| somatic clone (Zusman et al., 1993, Zusman et al., 1990)
Phenotype Manifest In
	abdominal 2 lateral longitudinal muscle 1 (Brown, 1994) abdominal 2 segment border muscle (Brown, 1994) abdominal 2 ventral longitudinal muscle 1 (Brown, 1994) abdominal 3 lateral longitudinal muscle 1 (Brown, 1994) abdominal 3 segment border muscle (Brown, 1994) abdominal 3 ventral longitudinal muscle 1 (Brown, 1994) abdominal 4 lateral longitudinal muscle 1 (Brown, 1994) abdominal 4 segment border muscle (Brown, 1994) abdominal 4 ventral longitudinal muscle 1 (Brown, 1994) abdominal 5 lateral longitudinal muscle 1 (Brown, 1994) abdominal 5 segment border muscle (Brown, 1994) abdominal 5 ventral longitudinal muscle 1 (Brown, 1994) abdominal 6 lateral longitudinal muscle 1 (Brown, 1994) abdominal 6 segment border muscle (Brown, 1994) abdominal 6 ventral longitudinal muscle 1 (Brown, 1994) abdominal 7 lateral longitudinal muscle 1 (Brown, 1994) abdominal 7 segment border muscle (Brown, 1994) abdominal 7 ventral longitudinal muscle 1 (Brown, 1994) adult cuticle \| somatic clone (Zusman et al., 1990) amnioserosa (Schock and Perrimon, 2003, Roote and Zusman, 1995, Narasimha and Brown, 2004) 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) cardial valve \| precursor (Pankratz and Hoch, 1995) central nervous system (Roote and Zusman, 1995) circular visceral muscle primordium \| maternal effect (Devenport and Brown, 2004) dorsal superficial trachea (Stark et al., 1997) dorsal trunk primordium (Boube et al., 2001) embryo \| dorsal closure stage, with mys^{D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) 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 (Li et al., 1998, Brown, 1994, Grinblat et al., 1994, Loer et al., 2008) embryonic/larval visceral branch (Boube et al., 2001) embryonic/larval visceral muscle & midgut (Devenport and Brown, 2004) embryonic dorsal epidermis (Brown, 1994) embryonic epidermis \| dorsal (Zusman et al., 1993) embryonic somatic muscle (Jani and Schock, 2007) extended germ band embryo (Roote and Zusman, 1995) extended germ band embryo \| germline clone (Martin-Bermudo et al., 1999) eye (Grinblat et al., 1994) eye \| somatic clone (Zusman et al., 1993) female germline cyst \| somatic clone (Bolivar et al., 2006) follicle cell \| somatic clone (Bolivar et al., 2006) gastric caecum (Brown, 1994) germ band (Schock and Perrimon, 2003) germ band, with mys^{D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) germ band, with mys^{S196F.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) germ layer \| embryonic stage (Li et al., 1998) haltere \| somatic clone (Zusman et al., 1990) interfollicle cell \| somatic clone (Bolivar et al., 2006) leg \| somatic clone (Zusman et al., 1990) midgut constriction (Roote and Zusman, 1995, Devenport and Brown, 2004, Brown, 1994) midgut primordium (Li et al., 1998) muscle attachment site (Prokop et al., 1998) muscle tendon junction, with mys^{804stop.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) muscle tendon junction, with mys^{D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) muscle tendon junction, with mys^{D807R.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) muscle tendon junction, with mys^{S196F.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) neuromuscular junction (Beumer et al., 1999) neuromuscular junction (with mys^olfC-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 (Roote and Zusman, 1995) tendon cell \| embryonic stage (Martin-Bermudo, 2000) tergite \| somatic clone (Zusman et al., 1990) terminal tracheal cell \| somatic clone (Levi et al., 2006) ventral nerve cord (Brown, 1994) 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 Approximately 47% of mys[11] mutant embryos, lacking both maternal and zygotic mys, fail to undergo germband retraction, while approximately 67% fail to complete dorsal closure. mys[11] mutant embryos exhibit a muscle detachment phenotype at stage 17, characteristic of a myotendinous junction failure at stage 16. (Pines et al., 2011) 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) mys^olfC-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 mys^b9/mys¹¹ larvae contain small, tightly clustered boutons surrounded by numerous mini-boutons. The neuromuscular junctions of mys^ts1/mys¹¹ larvae show no significant increase in bouton numbers. mys^b9/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 mys^b9/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. mys^ts1/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 mys^b9/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 mys^b9/mys¹¹ larvae. mys^ts1/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) cno^mis1 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-β_PS 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
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement Reference mys¹¹ is a suppressor of neuroanatomy defective phenotype of RhoGAPp190^{dsRNA.GAP.Scer\UAS}, Scer\GAL4^ey-OK107 (Billuart et al., 2001)
Phenotype Manifest In
Enhanced by
Statement Reference mys¹¹ has anterior midgut primordium phenotype, enhanceable \| maternal effect by Itgβν¹/Itgβν¹ (Devenport and Brown, 2004) mys¹¹ has embryonic/larval optic stalk phenotype, enhanceable by Fak^CG1/Fak56D[+] (Murakami et al., 2007) mys¹¹ has embryonic/larval visceral muscle & midgut phenotype, enhanceable by Itgβν¹/Itgβν¹ (Devenport and Brown, 2004) mys¹¹ has midgut constriction phenotype, enhanceable by Itgβν¹/Itgβν¹ (Devenport and Brown, 2004) mys¹¹ has salivary gland common duct primordium \| maternal effect phenotype, enhanceable \| maternal effect by Itgβν¹ (Devenport and Brown, 2004)
NOT Enhanced by
Statement Reference mys¹¹/mys⁸ has wing phenotype, non-enhanceable by pot[+]/pot^P3 (Walsh and Brown, 1998) mys¹¹ has circular visceral muscle primordium \| maternal effect phenotype, non-enhanceable by Itgβν¹/Itgβν¹ (Devenport and Brown, 2004)
Suppressed by
Statement Reference mys¹¹ has phenotype, suppressible by vn^Scer\UAS.cYa/Scer\GAL4^69B (Martin-Bermudo, 2000)
NOT suppressed by
Statement Reference mys¹¹ has anterior midgut primordium \| maternal effect phenotype, non-suppressible by Itgβν^EP2235/Scer\GAL4^48Y (Devenport and Brown, 2004) mys¹¹ has phenotype, non-suppressible by vn^Scer\UAS.cYa/Scer\GAL4^twi.PG/Scer\GAL4^how-24B/Scer\GAL4^how-24B (Martin-Bermudo, 2000) mys¹¹ has salivary gland common duct primordium \| maternal effect phenotype, non-suppressible by Itgβν^EP2235/Scer\GAL4^48Y (Devenport and Brown, 2004)
Enhancer of
Statement Reference mys¹¹/mys[+] is an enhancer of embryonic/larval optic stalk phenotype of Fak^CG1 (Murakami et al., 2007) mys¹¹/mys[+] is an enhancer of extended germ band embryo phenotype of EcR^{hs.T:Scer\GAL4} (Kozlova and Thummel, 2003)
Suppressor of
Statement Reference mys¹¹ is a suppressor of macrophage phenotype of PDZ-GEF^EP388, Scer\GAL4^srp (Huelsmann et al., 2006) mys¹¹ is a suppressor of macrophage phenotype of R^{V12.Scer\UAS.T:Hsap\MYC}, Scer\GAL4^srp (Huelsmann et al., 2006) mys¹¹ is a suppressor of mushroom body vertical lobe phenotype of RhoGAPp190^{dsRNA.GAP.Scer\UAS}, Scer\GAL4^ey-OK107 (Billuart et al., 2001)
Other
Statement Reference cno^mis1, mys¹¹ has wing vein phenotype (Miyamoto et al., 1995)
Additional Comments
Genetic Interactions
Statement Reference Fak56D^CG1 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\GAL4^srp>Gef26^EP388 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\GAL4^srp>R^{V12.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-ν^unspecified 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-ν^EP2235; Scer\GAL4^48Y. 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 EcR^{hs.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 vn^Scer\UAS.cYa in the tendon cells under the control of Scer\GAL4^69B can rescue the phenotype of mys¹¹ embryos (that lack both maternal and zygotic mys function), while expression of vn^Scer\UAS.cYa in the mesoderm under the control of both Scer\GAL4^twi.PG and Scer\GAL4^how-24B cannot. (Martin-Bermudo, 2000) The frequency of wing blisters seen in mys¹¹/mys⁸ flies is not dominantly enhanced by pot^P3. (Walsh and Brown, 1998)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Complements	mys^ts2 (Bunch et al., 1992) mys^ts3 (Bunch et al., 1992)
Fails to complement	mys^ts1 (Bunch et al., 1992)
Rescued by	mys¹¹/mys^G1 is rescued by mys^{Ubi-p63E.T:Avic\GFP-EYFP} (Ellis et al., 2011) mys¹¹ is rescued by mys^{D807R.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is rescued by mys^din (Grinblat et al., 1994) mys¹¹ is rescued by mys^{G792N.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is rescued by mys^{L211I.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is rescued by mys^rDEA (Grinblat et al., 1994) mys¹¹ is rescued by mys^rYYF (Grinblat et al., 1994, Li et al., 1998) mys¹¹ is rescued by mys^tZa (Li et al., 1998) mys¹¹ is rescued by mys^{Ubi-p63E.T:Avic\GFP-EYFP} (Pines et al., 2011) mys¹¹ is rescued by mys^{Y831F.Y843F.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is rescued by Scer\GAL4^Kr.PM/mys^din.Scer\UAS (Schock and Perrimon, 2003)
Partially rescued by	mys¹¹ is partially rescued by mys^4A.hs (Zusman et al., 1993) mys¹¹ is partially rescued by mys^4A (Zusman et al., 1993) mys¹¹ is partially rescued by mys^4B.hs (Zusman et al., 1993) mys¹¹ is partially rescued by mys^4B (Zusman et al., 1993) mys¹¹ is partially rescued by mys^{804stop.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is partially rescued by mys^{D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is partially rescued by mys^din.Scer\UAS/Scer\GAL4^48Y (Martin-Bermudo et al., 1999) mys¹¹ is partially rescued by mys^{L796N.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is partially rescued by mys^{N840A.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is partially rescued by mys^rDEA (Li et al., 1998) mys¹¹ is partially rescued by mys^rFFA (Li et al., 1998, Grinblat et al., 1994) mys¹¹ is partially rescued by mys^tZa (Zusman et al., 1993, Grinblat et al., 1994) mys¹¹ is partially rescued by Scer\GAL4^twi.PG/Scer\GAL4^how-24B/Scer\GAL4^how-24B/mys^din.Scer\UAS (Martin-Bermudo et al., 1999)
Not rescued by	mys¹¹/mys^G1 is not rescued by mys^{E810Q.E817Q.Ubi-p63E.T:Avic\GFP-EYFP} (Ellis et al., 2011) mys¹¹/mys^G1 is not rescued by mys^{N828A.Ubi-p63E.T:Avic\GFP-EYFP} (Ellis et al., 2011) mys¹¹ is not rescued by mys^{D807R.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is not rescued by mys^{S196F.T:Avic\GFP-EYFP.Ubi-p63E} (Pines et al., 2011) mys¹¹ is not rescued by mys^t1 (Li et al., 1998, Grinblat et al., 1994) mys¹¹ is not rescued by mys^t2 (Grinblat et al., 1994, Li et al., 1998)
Comments	The presence of mys[E810Q.E817Q.Ubi-p63E.T:Avic\GFP-EYFP] fails to rescue the germband retraction and dorsal closure defects of mys[11]/mys[G1] embryos, but partially rescues myotendinous junction defects. (Ellis et al., 2011) Approximately 5% of mys[11] mutant embryos expressing mys[Ubi-p63E.T:Avic\GFP-EYFP] fail to undergo germband retraction, indicating rescue. Expression of mys[Ubi-p63E.T:Avic\GFP-EYFP] rescues the dorsal closure defects seen in mys[11] mutant embryos. Expression of mys[Ubi-p63E.T:Avic\GFP-EYFP] rescues the myotendinous junction failure seen in mys[11] embryos. Expression of mys[D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E] partially rescues the germband retraction phenotype found in mys[11] embryos. However, the dorsal closure defects found in these embryos was not rescued and indeed in many cases appeared more severe. The mys[D19A.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 mys[D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E]. Expression of mys[S196F.T:Avic\GFP-EYFP.Ubi-p63E] fails to rescue both the germband retraction and dorsal closure phenotypes found in mys[11] embryos. The mys[S196F.T:Avic\GFP-EYFP.Ubi-p63E] transgene fails to rescue the muscle detachment phenotype seen in mys[11] embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type. Expression of mys[L211I.T:Avic\GFP-EYFP.Ubi-p63E] rescues both the germband retraction and dorsal closure phenotypes found in mys[11] embryos. The mys[L211I.T:Avic\GFP-EYFP.Ubi-p63E] transgene rescues the muscle detachment phenotype seen in mys[11] embryos. Expression of mys[G792N.T:Avic\GFP-EYFP.Ubi-p63E] rescues both the germband retraction and dorsal closure phenotypes found in mys[11] embryos. The mys[G792N.T:Avic\GFP-EYFP.Ubi-p63E] transgene rescues the muscle detachment phenotype seen in mys[11] embryos. Expression of mys[L796N.T:Avic\GFP-EYFP.Ubi-p63E] partially rescues the germband retraction phenotype and almost completely rescues the dorsal closure phenotype found in mys[11] embryos. The mys[L796N.T:Avic\GFP-EYFP.Ubi-p63E] transgene rescues the muscle detachment phenotype seen in mys[11] embryos. Expression of mys[804stop.T:Avic\GFP-EYFP.Ubi-p63E] partially rescues the germband retraction phenotype and fails to rescue the dorsal closure phenotype found in mys[11] embryos. Indeed in many cases the dorsal closure defects appear more severe. The mys[804stop.T:Avic\GFP-EYFP.Ubi-p63E] transgene fails to rescue the muscle detachment phenotype seen in mys[11] embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type. Expression of mys[D807R.T:Avic\GFP-EYFP.Ubi-p63E] rescues both the germband retraction and dorsal closure phenotypes found in mys[11] embryos. The mys[D807R.T:Avic\GFP-EYFP.Ubi-p63E] transgene fails to rescue the muscle detachment phenotype seen in mys[11] embryos, with the myotendinous junctions appearing shorter and smaller overall, compared to wild-type. Expression of mys[Y831F.Y843F.T:Avic\GFP-EYFP.Ubi-p63E] rescues the germband retraction phenotype but exacerbates the dorsal closure phenotype found in mys[11] embryos. The mys[Y831F.Y843F.T:Avic\GFP-EYFP.Ubi-p63E] transgene rescues the muscle detachment phenotype seen in mys[11] embryos. Expression of mys[N840A.T:Avic\GFP-EYFP.Ubi-p63E] partially rescues both the germband retraction and dorsal closure phenotypes found in mys[11] embryos. The mys[N840A.T:Avic\GFP-EYFP.Ubi-p63E] transgene partially rescues the muscle detachment phenotype seen in mys[11] 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 mys^din.Scer\UAS expressed under the control of Scer\GAL4^48Y, although there is a small delay in migration. The visceral mesoderm and germband retraction defects are not rescued in these embryos. mys^din.Scer\UAS expressed under the control of both Scer\GAL4^twi.PG and Scer\GAL4^how-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 mys^tZa or mys^rYYF rescues embryonic abnormalities of mutants. Many embryonic abnormalities are not rescued by mys^t1 (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 mys^rDEA or mys^rFFA. mys^rDEA also rescues defects in midgut migration and elongation and in maintaining closure of the embryonic cuticle. (Li et al., 1998)
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	Endoderm migrates normally over the visceral mesoderm. (Reuter et al., 1993) No PSβ protein. (Wilcox et al., 1989)
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Synonyms & Secondary IDs ( 8 )
Reported As
Symbol Synonym	l(1)mys^xG43 (Reuter et al., 1993, Wilcox et al., 1989, ) l(1)mys^XG43 (Zusman et al., 1990, Volk et al., 1990) myospheroid^XG43 (Narasimha and Brown, 2004, Narasimha and Brown, 2004, Levi et al., 2006) mys¹¹ (Bolivar et al., 2006) mys^XG43 (Devenport and Brown, 2004, Torgler et al., 2004, Kozlova and Thummel, 2003, Clark et al., 2003, Bradley et al., 2003, Brown et al., 2002, Schock and Perrimon, 2003, Jannuzi et al., 2002, Billuart et al., 2001, Boube et al., 2001, Zervas et al., 2001, Martin-Bermudo and Brown, 2000, Martin-Bermudo, 2000, Martin-Bermudo et al., 1999, Beumer et al., 1999, Martin-Bermudo and Brown, 1999, Walsh and Brown, 1998, Prokop et al., 1998, Li et al., 1998, Stark et al., 1997, Hoch and Pankratz, 1996, Martin-Bermudo and Brown, 1996, Roote and Zusman, 1996, Longley and Ready, 1995, Roote and Zusman, 1995, Miyamoto et al., 1995, Pankratz and Hoch, 1995, Fogerty et al., 1994, Brown, 1994, Brown et al., 1993, Grinblat et al., 1994, Zusman et al., 1993, Bunch et al., 1992, Wahlstrom et al., 2006, Huelsmann et al., 2006, Bokel et al., 2005, Devenport et al., 2007, Murakami et al., 2007, Volohonsky et al., 2007, Becam et al., 2005, Subramanian et al., 2007, Jani and Schock, 2007, Loer et al., 2008, Loer et al., 2008, Rushton et al., 2009, Bolivar et al., 2006, Haghayeghi et al., 2010, Tanentzapf et al., 2006, Zervas et al., 2011, Bahri et al., 2010, Pines et al., 2011, Ellis et al., 2011) mys^xg43 (Beumer et al., 2002) mys^xG43 (Volk, 1992) βPS integrin^- (Narasimha and Brown, 2004)
Name Synonym
Secondary FlyBase IDs

References ( 63 )

Generate a list of	All references relating to this allele ( 63 )

List References by type	Research paper ( 60 ) Supplementary material ( 2 ) Review ( 1 )
Recent research papers ( 4 )
	Bossing et al., 2012, Dev. Cell 23(2): 433--440 Disruption of Microtubule Integrity Initiates Mitosis during CNS Repair. [FBrf0219196] Ellis et al., 2011, J. Cell Sci. 124(11): 1844--1856 In vivo functional analysis reveals specific roles for the integrin-binding sites of talin. [FBrf0213701] Pines et al., 2011, Dev. Dyn. 240(1): 36--51 Distinct regulatory mechanisms control integrin adhesive processes during tissue morphogenesis. [FBrf0212613] Zervas et al., 2011, J. Cell Sci. 124(8): 1316--1327 A central multifunctional role of integrin-linked kinase at muscle attachment sites. [FBrf0213331] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2011 Show reviews ...

Allele Dmel\mys11

Allele Dmel\mys¹¹