Inversion breakpoint is within the coding region between nucleotides 1405 and 1848.
Slight irregularities in the apical surface of the salivary gland are seen at stage 12 in mutant embryos. By stage 14/15 the salivary gland tube is buckled.
Adult mewM6 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; enteroendocrine cell/enterocyte ratio is unaffected and intestinal stem cells show no obvious signs of apoptosis.
mewM6 mutant class IV da neurons (generated using the MARCM system under the control of Scer\GAL4109(2)80) have significantly more dendrites that are enclosed in the epidermis rather than attached to the ECM in comparison with wild-type. They also exhibit an increased number of dendritic crossings, and 86.97% of these are non-contacting as the dendrites are in a different apical-basal plane.
mewM6 follicle cell clones organize stress fibres similar to wild type, but have elevated levels of basal F-actin. These cells do not display cell shape defects.
Hemizygous mewM6/Y mutant embryos display muscle detachments in only few segments.
Homozygous embryos show axon guidance defects characteristic of increased fasciculation in the ISNb pathway (82.3% of hemisegments), in the SNa pathway (71.8% of hemisegments) and in the central nervous system (55.8% of hemisegments).
mewM6 dorsal branch terminal cell clones do not cause any detectable defects in terminal cell morphology.
mewM6 mutant embryos show salivary gland guidance defects. A minority of these mutants have salivary glands that lie parallel to the CNS midline, as in wild type. 35% of these mewM6 embryos possess at least one gland that curves medially towards the midline, while a further 35% have at least one gland that curves laterally away from the midline.
Salivary cells invaginate and move dorsally to the visceral mesoderm in mutant embryos, but fail to migrate away from the turning point (the point where the cells turn to reorient their movement posteriorly in wild-type embryos). The salivary glands are often bent and mispositioned in late stage mutant embryos. The length and diameter of the mutant salivary glands is similar to wild type.
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.
The continuous layer of visceral mesoderm that normally surrounds the gut is moderately disrupted in homozygous embryos.
Endodermal midgut cells of homozygous embryos show a modest delay of approximately 30 minutes in midgut migration, so that anterior and posterior midgut cells do not contact each other until stage 13 when wild-type cells have already fused. The endodermal cells still send projections towards the visceral mesoderm, as in wild type. The arrangement of the visceral mesoderm cells is normal in homozygous embryos.
Homozygous embryos have an increased rate of axon errors in the central and peripheral nervous systems compared to wild-type.
Homozygous embryos do not have any ultrastructural defects at muscle attachment sites.
Most homozygous larvae die during the first or second instar stages.
In 30 and 36 hour after pupariation (AP) dorsal clones are associated with pronounced matrix-filled blisters. Small clones (fewer than 150 cells) in the wing are often wild type or have a weak phenotype, even if on the dorsal surface.
Mitotic clones in the eye exhibit photoreceptor disorganisation and holes resulting in spaces between and within ommatidial units. Disruption is mild and defects are often restricted to the basal surface of the retina.
Midgut does not elongate into the tubular structure but there are no obvious defects in somatic muscle morphogenesis. Dorsal herniation is not observed in homozygotes or double mutant combinations with ifk27e and ifB4. Large dorsal wing clones cause wing blisters, small clones of approximately 5 cells have no phenotype and clones of 100 cells show a mild phenotype such as wrinkles confined to one end of the clone. Large dorsal wing clones cause wing blisters, small clones of approximately 5 cells have no phenotype and clones of 100 cells show a mild phenotype such as wrinkles confined to one end of the clone. Clones in the eye exhibit photoreceptor disorganisation.
Clonal analysis reveals that lack of mew has no discernible effect on germ cell development. Mutant embryos show a distinct and reproducible separation between the ectodermal and mesodermal tissue layers of the germband, though the separation is not complete. Midgut primordia meet and initiate fusion at least 1 to 2 hours after wild type embryos would. Visceral mesoderm appears normal. Midgut constrictions partially form.
mewM6 has abnormal neuroanatomy phenotype, enhanceable by sli2
mewM6 has lethal phenotype, suppressible by ifm8.UAS/Scer\GAL448Y
mewM6 has lethal phenotype, suppressible by Scer\GAL448Y/ifC.UAS
mewM6 has lethal phenotype, suppressible by if::mewUAS.cMBb/Scer\GAL448Y
mewM6 has lethal phenotype, suppressible by if::mewUAS.cMBa/Scer\GAL448Y
mewM6 has lethal phenotype, suppressible by Scer\GAL448Y/ifUAS.cMBa
mewM6 is an enhancer of abnormal neuroanatomy phenotype of sliunspecified
RetC168/Ret[+], mewM6 has abnormal neuroanatomy phenotype
LanA9-32, mew[+]/mewM6 has abnormal neuroanatomy | third instar larval stage phenotype
mew[+]/mewM6, wb09437 has abnormal neuroanatomy | third instar larval stage phenotype
Scer\GAL4109(2)80, mewM6, mys1/mys[+] has abnormal neuroanatomy | somatic clone | third instar larval stage phenotype
LanB2MB04039, mew[+]/mewM6 has abnormal neuroanatomy | third instar larval stage phenotype
Df(3L)Exel6083/+, mewM6 has abnormal neuroanatomy | dominant phenotype
mewM6, mys[+]/mysolfC-x17 has abnormal smell perception phenotype
mewM6, mysolfC-x3/mys[+] has abnormal smell perception phenotype
mewM6, mysolfC-x17 has abnormal smell perception phenotype
mewM6, mysolfC-x3 has abnormal smell perception phenotype
mewM6 has adult posterior midgut epithelium | somatic clone phenotype, non-enhanceable by ifk27e/ifk27e
mewM6 has phenotype, suppressible by if::mewUAS.cMBb/Scer\GAL448Y
mewM6 has retina | somatic clone phenotype, suppressible by ifC.UAS/Scer\GAL4hs.PB
mewM6 has retina | somatic clone phenotype, suppressible by ifm8.UAS/Scer\GAL4hs.PB
mewM6 has adult posterior midgut epithelium | somatic clone phenotype, non-suppressible by ifk27e/ifk27e
mewM6 has embryonic/larval visceral tracheal branch phenotype, non-suppressible by Scer\GAL4btl.PS/ifUAS.cMBa
mewM6 has embryonic/larval midgut | embryonic stage phenotype, non-suppressible by Scer\GAL448Y/ifUAS.cMBa
mewM6 has wing | somatic clone phenotype, non-suppressible by Scer\GAL4684/ifC.UAS
mewM6 is an enhancer of muscle attachment site phenotype of TspΔ79
mewM6 is an enhancer of presumptive embryonic salivary gland phenotype of fra3/fra4
mewM6 is an enhancer of fascicle phenotype of sliunspecified
mew[+]/mewM6 is a non-enhancer of heart primordium phenotype of sli2
RetC168/Ret[+], mewM6 has larval multidendritic class IV neuron phenotype
LanA9-32, mew[+]/mewM6 has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype
mew[+]/mewM6, wb09437 has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype
Scer\GAL4109(2)80, mewM6, mys1/mys[+] has larval dorsal multidendritic neuron ddaC | somatic clone | third instar larval stage phenotype
LanB2MB04039, mew[+]/mewM6 has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype
βTub85Dn, mewM6 has presumptive embryonic salivary gland phenotype
Df(3L)Exel6083/+, mewM6 has larval intersegmental nerve phenotype
Df(3L)Exel6083/+, mewM6 has presumptive embryonic/larval central nervous system phenotype
Df(3L)Exel6083/+, mewM6 has larval segmental nerve phenotype
ifk27e, mewM6 has terminal tracheal cell | somatic clone phenotype
fra3/fra4, mewM6 has presumptive embryonic salivary gland phenotype
mewM6, sogEP7 has wing vein | dorsal | somatic clone phenotype
mewM6, sog[+]/sogEP7 has wing vein | dorsal | somatic clone phenotype
mewM6, scb2 has embryonic/larval midgut | embryonic stage phenotype
ifB4, mewM6 has embryonic/larval midgut | embryonic stage phenotype
ifB4, mewM6 has somatic muscle cell phenotype
ifk27e, mewM6 has somatic muscle cell phenotype
Reduced maintenance phenotype of adult mewM6/mewM6, ifk27e/ifk27e double mutant intestinal stem cell clones is partially rescued by expression of mewUAS.cWa under the control of Scer\GAL4Act.PU in these clones.
22.62% of mewM6/mys1 mutant class IV da dendrites (generated using the MARCM system under the control of Scer\GAL4109(2)80) are enclosed in the epidermis rather than attached to the ECM. This compares to 4.09% and 4.18% in mys1/+ and mewM6/+ respectively.
mewM6/wb09437 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendrite length that is enclosed within the epidermis rather than attached to the ECM. The amount of enclosed dendrite seen in each heterozygote is similar to wild type.
mewM6/LanA9-32 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendrite length that is enclosed within the epidermis rather than attached to the ECM. The amount of enclosed dendrite seen in each heterozygote is similar to wild type.
mewM6/LanB2MB04039 mutant third instar larvae show a mild but statistically significant increase in the proportion of dorsal midline ddaC dendrite length that is enclosed within the epidermis rather than attached to the ECM. The amount of enclosed dendrite seen in each heterozygote is similar to wild type.
Hemizygous mewM6 mutant embryos that are also heterozygous for Tspunspecified develop a weak muscle detachment phenotype affecting a small number of longitudinal muscles.
Hemizygous mewM6/Y mutant embryos that are also homozygous for TspΔ79 display only a mild enhancement of the TspΔ79 single mutant muscle detachment phenotype.
mewM6/+ ; Df(3L)Exel6083/+ double heterozygotes show axon guidance defects characteristic of increased fasciculation in the ISNb pathway (73.6% of hemisegments), in the SNa pathway (55.3% of hemisegments) and in the central nervous system (40.5% of hemisegments). These defects are not seen in either single heterozygote.
Small mys10 somatic clones in the wing generated a sogEP7 background cause a distinctive vein phenotype: Dorsal clones located in the proximity of veins bend and displace the veins towards the clone, so that this vein runs along and outside the clone boundary. This vein shifting phenotype is observed for all longitudinal veins. However, clones that cross over a vein generate no phenotype, and neither do clones generated at a distance of three or more cells from a vein. Small ventrally located clones have no effect on vein formation.
When tested in the odour-induced jump-test, double heterozygotes of mewM6 and either mysolfC-x3 or mysolfC-x17 show reduced responses to both ethyl acetate and iso-amyl acetate.
In mewM6/+ sli2/+ double heterozygous mutants the frequency of midline guidance errors is increased over the level observed in mewM6 homozygous mutants. Less than 10% of segments revealed midline guidance errors in mewM6/+ sli2/+ embryos. The frequency of midline crossing is much higher in mewM6/Y;sliunspecified/+ and also involves more lateral tracts.
The midgut phenotype is enhanced in ifB4 mewM6 double mutant embryos. ifScer\UAS.cMBa does not rescue the migration defects of the midgut endodermal cells in mewM6 embryos, when expressed under the control of Scer\GAL448Y. mewM6 scb2 double mutant embryos show a strong defect in the migration of the endodermal midgut cells, with a delay in migration of approximately 2 hours (similar to that observed in embryos lacking both maternal and zygotic mys function).
ifScer\UAS.cMBa, ifC.Scer\UAS or ifm8.Scer\UAS partially rescue the first instar lethality of mewM6 homozygotes when expressed using Scer\GAL448Y, although the animals do not survive past the second larval instar stage. if::mewScer\UAS.cMBa partially rescues the first instar lethality of mewM6 homozygotes when expressed using Scer\GAL448Y. The first instar lethality of mewM6 homozygotes is rescued by if::mewScer\UAS.cMBb expressed using Scer\GAL448Y.
Scer\GAL4684 induced expression of ifC.Scer\UAS fails to rescue the blistering phenotype.
Expression of ifC.Scer\UAS and ifm8.Scer\UAS also rescues the mutant phenotype in most of the clones with similar efficiency to mewScer\UAS.cWa.
Double mutants for mew and if have a midgut phenotype as severe as that of mys mutants. Somatic muscle appears normal. Dorsal hole and U-shaped cuticle of mys mutants are not observed in mew or if mutants. Double mutants between mew498, mew023 or mewM6 and ifk27e or ifB4 do not show the twisted germband, amnioserosal detachment, dorsal movement of germband, dorsal hole and U-shaped embryo phenotypes of mys mutants, but do show early muscle detachments, as seen for mys mutants.
mewM6 is rescued by Scer\GAL4btl.PS/mewUAS.cWa
mewM6 is rescued by mewUAS.cMBa/Scer\GAL448Y
mewM6 is rescued by mewUAS.cMBa/Scer\GAL448Y
mewM6 is rescued by mewUAS.cMBb/Scer\GAL448Y
mewM6 is rescued by Scer\GAL4684/mewUAS.cWa
This lethality is rescued by mewScer\UAS.cMBa or mewScer\UAS.cMBb expressed using Scer\GAL448Y, with some larvae developing up to the third instar stage, although they do not develop into adults.
Scer\GAL4684 induced expression of mewScer\UAS.cWa rescues dorsal clones completely.
Scer\GAL4hs.PB mediated expression of mewScer\UAS.cWa in the clones completely rescues the disorganised photoreceptor phenotype in 85% of the clones and partially in the remaining clones.