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General Information
Symbol
Dmel\mewM6
Species
D. melanogaster
Name
FlyBase ID
FBal0039653
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Inversion breakpoint is within the coding region between nucleotides 1405 and 1848.

Caused by aberration
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

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.

mewM6 mutant embryos exhibit thinning of the longitudinal fascicles (visible with Fas2), with occasional defasciculation defects.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

mewA1-5/mewM6 has visible phenotype, enhanceable by pot[+]/potP3

Suppressed by
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

mew[+]/mewM6 is a suppressor of visible | dominant phenotype of sogEP7

mew[+]/mewM6 is a suppressor of visible | dominant phenotype of sogEP11

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

mewM6 has muscle attachment site phenotype, enhanceable by Tsp[+]/Tspunspecified

mewM6 has fascicle phenotype, enhanceable by sli2

mewA1-5/mewM6 has wing phenotype, enhanceable by pot[+]/potP3

NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

mew[+]/mewM6 is a non-enhancer of heart primordium phenotype of sli2

Suppressor of
Statement
Reference

mew[+]/mewM6 is a suppressor of wing vein phenotype of sogEP7

mew[+]/mewM6 is a suppressor of wing vein phenotype of sogEP11

NOT Suppressor of
Statement
Reference

mew[+]/mewM6 is a non-suppressor of eye phenotype of Atg1K.GMR

Other
Statement
Reference

mewM6, mysb45 has neuron & eye photoreceptor cell phenotype

Additional Comments
Genetic Interactions
Statement
Reference

RetC168 mewM6 transheterozygous third instar larvae exhibit defects in class IV dendritic arborizing neuron dendrite crossing and a substantial loss of dendrite-ECM interaction. No phenotypes are observed in either heterozygote alone.

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.

Embryos trans-heterozygous for βTub85Dn and mewM6 exhibit salivary gland migration defects.

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.

mewM6, ifk27e double mutant dorsal branch terminal cell clones show a loss of terminal branches and an increase in lumen density and complexity in the remaining branches.

mewM6/+; sli2/+ embryos do not show defects in heart formation.

mewM6 mysb45 double heterozygotes show displacement of photoreceptor nuclei in the retina in 3% of cases.

In mewM6/Y; fra3/fra4 double mutant embryos, the misguided salivary gland phenotype is modified, compared to that of each single mutant. Like fra3/fra4 mutants, the majority (75%) of misguided glands curve laterally, but levels of penetrance are high, similar to mewM6/Y single mutants.

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.

Salivary glands in mewM6 scb2 mutant embryos are indistinguishable from those in mewM6 embryos.

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).

The frequency of wing blisters seen in mewA1-5/mewM6 flies is dominantly enhanced by potP3.

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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

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.

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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (32)