Deletion of nucleotides 2110-2222, resulting in a frame shift after amino acid residue 704.
bouton & neuromuscular junction
bouton & neuromuscular junction & abdominal ventral longitudinal muscle 1
embryonic/larval visceral muscle & midgut
neuromuscular junction & abdominal lateral longitudinal muscle 1
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.
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.
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.
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.
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 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.
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.
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.
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.