|Feature type||allele||Associated gene||Dmel\mys|
|Also Known As||mysXG43, l(1)mysxG43, myospheroidXG43|
|Map ( GBrowse )|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
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Controlled Vocabulary Terms
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Deletion of nucleotides 2110-2222, resulting in a frame shift after amino acid residue 704.
|Phenotype Manifest In|
bouton & neuromuscular junction
bouton & neuromuscular junction & abdominal ventral longitudinal muscle 1
embryonic/larval visceral muscle & midgut
neuromuscular junction & abdominal lateral longitudinal muscle 1
Approximately 47% of mys mutant embryos, lacking both maternal and zygotic mys, fail to undergo germband retraction, while approximately 67% fail to complete dorsal closure. mys mutant embryos exhibit a muscle detachment phenotype at stage 17, characteristic of a myotendinous junction failure at stage 16.
Homozygous embryos show a detached muscle phenotype.
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.
Zygotic mys11 embryos do not show a phenotype in macrophage shape or migration.
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.
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.
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.
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.
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.
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.
Mutant embryos show dorsal herniation.
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.
The tendon matrix appears disorganised in homozygous embryos derived from homozygous females and the muscles detach.
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.
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.
Attachment of muscles to the epidermis is disturbed in stage 16 homozygous embryos.
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.
Cardiac arrest phenotype, foregut cells are clustered at the top of the proventriculus and cannot migrate inside to form the cardiac valve.
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.
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.
Embryos die with a dorsal hole in the cuticle. In clones, blisters form in the wing, and ommatidia are disorganized.
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.
No anti-βPS staining at muscle attachment sites.
Characteristic membranal localisation MSP-300, and concentration at attachment sites is not prominent in mys11.
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.
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.
|Phenotype Manifest In|
|NOT Enhanced by|
|NOT suppressed by|
mys11 has anterior midgut primordium | maternal effect phenotype, non-suppressible by ItgβνEP2235/Scer\GAL448Y
mys11 has phenotype, non-suppressible by vnScer\UAS.cYa/Scer\GAL4twi.PG/Scer\GAL4how-24B/Scer\GAL4how-24B
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.
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.
Homozygous mys11 follicle cell or germ-line clones that are induced in homozygous βInt-νunspecified females do not result in oocyte mislocalisation.
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.
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/+.
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.
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Not rescued by|
The presence of mys[E810Q.E817Q.Ubi-p63E.T:Avic\GFP-EYFP] fails to rescue the germband retraction and dorsal closure defects of mys/mys[G1] embryos, but partially rescues myotendinous junction defects.
Approximately 5% of mys 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 mutant embryos. Expression of mys[Ubi-p63E.T:Avic\GFP-EYFP] rescues the myotendinous junction failure seen in mys embryos. Expression of mys[D19A.S194A.T:Avic\GFP-EYFP.Ubi-p63E] partially rescues the germband retraction phenotype found in mys 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 embryos. The mys[S196F.T:Avic\GFP-EYFP.Ubi-p63E] transgene fails to rescue the muscle detachment phenotype seen in mys 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 embryos. The mys[L211I.T:Avic\GFP-EYFP.Ubi-p63E] transgene rescues the muscle detachment phenotype seen in mys embryos. Expression of mys[G792N.T:Avic\GFP-EYFP.Ubi-p63E] rescues both the germband retraction and dorsal closure phenotypes found in mys embryos. The mys[G792N.T:Avic\GFP-EYFP.Ubi-p63E] transgene rescues the muscle detachment phenotype seen in mys 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 embryos. The mys[L796N.T:Avic\GFP-EYFP.Ubi-p63E] transgene rescues the muscle detachment phenotype seen in mys 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 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 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 embryos. The mys[D807R.T:Avic\GFP-EYFP.Ubi-p63E] transgene fails to rescue the muscle detachment phenotype seen in mys 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 embryos. The mys[Y831F.Y843F.T:Avic\GFP-EYFP.Ubi-p63E] transgene rescues the muscle detachment phenotype seen in mys embryos. Expression of mys[N840A.T:Avic\GFP-EYFP.Ubi-p63E] partially rescues both the germband retraction and dorsal closure phenotypes found in mys embryos. The mys[N840A.T:Avic\GFP-EYFP.Ubi-p63E] transgene partially rescues the muscle detachment phenotype seen in mys 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.
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.
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.
|Stocks ( 0 )|
|Notes on Origin|
Endoderm migrates normally over the visceral mesoderm.
No PSβ protein.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 8 )|
(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)
|Secondary FlyBase IDs|
|References ( 63 )|
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|Recent research papers ( 4 )|
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