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General Information
Symbol
Dmel\exe1
Species
D. melanogaster
Name
FlyBase ID
FBal0031224
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ex-lacZ
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
deletion
Linked to:
HindIII-HindIII restriction fragment
Comment:

Approximate mapping of exe1 deletion to a restriction fragment; exe1 consists of a partial excision of the original P{lacW}ex697 insert plus removal of 3-12kb of flanking genomic sequence; position of restriction fragment on reference sequence inferred by FlyBase curator

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of a P{lacW} insertion that leaves behind the Ecol\lacZ gene.

Small deletion that removes 3-12kb of genomic DNA, including the first ex exon.

Insertion components
P{?lacW}exe1
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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

The relative size of somatic MARCM clones mutant for exe1 in third instar larval wing discs is significantly increased compared to control clones in wild-type discs.

Adult eyes containing exe1 homozygous somatic clones (induced by the eyFLP method) display overgrowth and folding phenotype not only in the eyes but also at the base of antennae.

exe1/+ does not have any affect on cell growth or proliferation in the adult posterior midgut, as compared to controls.

exe1/exe1 eyes (created by the EGUF method in otherwise heterozygous animals) contain significantly increased number of interomatidial cells (IOC) in the pupal retina compared to wild-type and the adult eyes are smaller and misshapen.

exe1/exe1 mutants rarely survive to third instar larval stage (but never to adulthood) and the survivors display decreased number of photoreceptor cells in the eye disc compared to wild-type.

The wing discs of exe1/exAP50 transheterozygotes are overgrown compared to controls.

exe1/exe1 mosaic adult wings are enlarged in size relative to controls. exe1/exe1 mosaic female heads exhibit both head and eye overgrowth as compared to controls.

Cells in homozygous clones in the wing disc accumulate F-actin near the apical surface.

exe1 mutant larvae show a decrease in the number of glial cells in the eye disc and a lack of glial overgrowth.

Eyes that are partially homozygous for exe1 (generated using the eyFLP method without cell lethal) show mild overgrowth compared to controls.

Pupal retinae composed of homozygous exe1 mutant cells show an increase in the number of interommatidial cells.

exe1 homozygous mutant clones generated in the male germline develop normally. 16 cells are observed per cyst, and cell size and morphology are indistinguishable from neighbouring control cells. However, non-autonomous germline over-proliferation is observed in non-mutant spermatogonial cysts.

exe1 mutant wing discs collected 36-48 hours after the L2-L3 molt are overgrown.

exe1 mutants do not exhibit any defect in photoreceptor differentiation.

Mutant exe1 clones, generated through FLP-induced recombination are significantly larger than their wild-type twin-spots at the larval stage.

exe1 pupal retinas exhibit an increase in secondary cells that are normally eliminated by apoptosis (approximately 8 in exe1 clones, compared to 6 in wild-type).

Somatic clones of homozygous exe1 tissue in the eye exhibit ommatidial chirality inversions, misrotations and minor defects in photoreceptor differentiation. Somatic clones in the pupal imaginal disc produces a disruption of the well-ordered pattern of R3/R4 photoreceptor precursor cells. Clones also exhibit a significant growth advantage over the wild-type counterparts in larval and pupal discs, and in the adult eye. In the case of large clones the tissue protrudes out of the plane of the disc. Homozygous exe1 animals survive until the pharate adult stage. The eye discs are disproportionately large in comparison with the antennal discs of the same complex, reaching several times the size of wild-type larvae. Anterior regions of mutant discs lose their 'flat' character, leading to the formation of additional tissue flaps. In these discs the morphogenetic furrow moves across the mutant tissue and cell fate determination does take place.

Clonal analysis revealed no effect on tissues other than the wing. Mutant clones generated 3-5 days AEL are more than twice as large as their wild type twins, but show no significant differences depending on the position in the wing. ex function is not required at or after 5-6 days AEL.

Pharate adults have a massive head, wing and leg defects. Most common leg defect is missing distal tarsal segments including claw organ, with the remaining proximal tarsal segments have supernumerary bristles. Wing disc of third instar larvae is enlarged, and by day 5 has formed an extra fold. Overgrowth also occurs in the haltere discs, and the eye disc and leg discs show signs of degeneration.

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

exe1 has visible | somatic clone phenotype, enhanceable by kibradel

Suppressed by
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

exe1 is an enhancer of visible | somatic clone phenotype of kibradel

ex[+]/exe1 is an enhancer of partially lethal - majority die phenotype of ft8/ftG-rv

ex[+]/exe1 is an enhancer of visible phenotype of dshhs.sev.B

exe1 is an enhancer of visible | recessive phenotype of Mer3

Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

exe1 has eye | somatic clone phenotype, enhanceable by kibradel

exe1 has ommatidium | somatic clone phenotype, enhanceable by kibradel

NOT Enhanced by
Statement
Reference

exe1 has phenotype, non-enhanceable by Rho1V14.sev

exe1 has phenotype, non-enhanceable by Rac1V12.hs.sev

exe1 has phenotype, non-enhanceable by fzhs.sev

Suppressed by
NOT suppressed by
Statement
Reference

exe1 has eye | somatic clone | adult stage phenotype, non-suppressible by Ack10b/Ack10b

exe1 has antenna | somatic clone | adult stage phenotype, non-suppressible by Ack10b/Ack10b

exe1 has wing disc | larval stage phenotype, non-suppressible by dGC13

exe1 has phenotype, non-suppressible by Rho1V14.sev

exe1 has phenotype, non-suppressible by Rac1V12.hs.sev

exe1 has phenotype, non-suppressible by fzhs.sev

Enhancer of
Statement
Reference

ex[+]/exe1 is an enhancer of wing phenotype of pydtam/pydex147

exe1 is an enhancer of eye | somatic clone phenotype of kibradel

exe1 is an enhancer of ommatidium | somatic clone phenotype of kibradel

ex[+]/exe1 is an enhancer of ommatidium phenotype of dshhs.sev.B

ex[+]/exe1 is an enhancer of eye phenotype of dshhs.sev.B

exe1 is an enhancer of adult cuticle & head phenotype of Mer3

NOT Enhancer of
Statement
Reference

exe1 is a non-enhancer of phenotype of Rho1V14.sev

exe1 is a non-enhancer of phenotype of fzhs.sev

exe1 is a non-enhancer of phenotype of Rac1V12.hs.sev

Suppressor of
NOT Suppressor of
Statement
Reference

exe1 is a non-suppressor of phenotype of Rho1V14.sev

exe1 is a non-suppressor of phenotype of Rac1V12.hs.sev

exe1 is a non-suppressor of phenotype of fzhs.sev

Other
Additional Comments
Genetic Interactions
Statement
Reference

The increased relative size of somatic MARCM clones mutant for exe1 in third instar larval wing discs (as compared to wild-type clones in control discs) is suppressed by expression of kibraScer\UAS.P\T.cGa in the mutant clones (driven by Scer\GAL4tub.PU), which on its own produces clones of reduced size.

The overgrowth phenotype observed in adult eye and antennae containing exe1 homozygous mutant somatic clones (induced by the eyFLP method) is not changed when the clones are induced in Ack10b/Ack10b mutant background or when they also express AckScer\UAS.T:SV5\V5 under the control of Scer\GAL4Ubi.PU.

exe1/+ fully suppresses the reduced growth seen in posterior midgut wild type clones when in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones, and suppresses the growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones.

Double homozygous ft8, exe1 clones generated using the eyFLP system result in substantial overgrowth of the head, particularly in the ptilinum.

The supernumerary inter-ommatidial cells in the pupal retina as well as the smaller size and altered eye shape in adults characteristic for exe1/exe1 eyes (created by the EGUF method in otherwise heterozygous animals) can be suppressed by combination with ZyxΔ41/ZyxΔ41.

The low survival rate of exe1/exe1 mutants to third instar larval stage can be improved by combination with ZyxΔ41/ZyxΔ41 and some of the double mutants can survive even to adulthood. The decreased number of photoreceptor cells in the eye discs characteristic for exe1/exe1 mutants is also restored in the surviving exe1;ZyxΔ41 double mutant third instar larvae.

The overgrowth of the wing discs characteristic for exe1/exAP50 transheterozygotes can be suppressed by combination with ZyxΔ41/ZyxΔ41.

tai61G1/tai61G1, exe1/exe1 mosaic adult wings are smaller than exe1/exe1 mosaic wings, although the wings are still a broader shape than controls; tai61G1/tai61G1, exe1/exe1 clones in the L3 wing disc appear smaller than age-matched exe1/exe1 clones; tai61G1/tai61G1, exe1/exe1 mosaic heads have suppressed head and eye overgrowth as compared to exe1/exe1 clones.

exe1/exe1, kibraΔ32/+ egg chambers develop a multilayered follicle cell epithelium.

Wings from pydex147/pydtam flies are broader compared to control wings, and this phenotype is enhanced in a exe1/+ background.

Expression of ykiNIG.4005R under the control of Scer\GAL4unspecified in exe1 clones in the wing disc does not prevent apical accumulation of F-actin in the mutant cells.

Pupae with mosaic heads that are largely doubly mutant for exe1/exe1 and kibra1/kibra3 (clones induced using the eyFLP method without cell lethal) do not eclose and normal head structures are displaced by overgrown tissue.

exe1 kibra1 double mutant clones in the eye imaginal disc are very large and invariably adopt a rounded shape.

Pupal retinae composed of crb82-04 exe1 double mutant cells show a similar number of interommatidial cells as do the single mutants.

exe1 ; kibradel double mutant clones in the eye show a more severe eye overgrowth phenotype and a greater number of interommatidial cells per ommatidium than is seen in either single mutant.

dmScer\UAS.cZa overexpression clones (under the control of Scer\GAL4hh.PU) found in the posterior of the wing disc strongly enhance the proliferative activity of exe1 mutant cells. In addition these cells are larger in dmScer\UAS.cZa clones than in a wild-type background.

exe1 allows recovery of Df(1)su(s)R194/+ clones in the adult eye in animals with mosaic eyes containing two genotypes of cells with respect to RpL36; cells which are Df(1)su(s)R194/+ and cells in which the haplo-insufficiency of Df(1)su(s)R194/+ for RpL36 has been rescued by RpL36+t4 (in a wild-type background the Df(1)su(s)R194/+ clones are eliminated by cell competition and are not seen in the adult eye in these animals).

dGC13 does not suppress the wing disc overgrowth seen in exe1 mutant larvae.

Somatic clones homozygous for Mer4 and exe1 in the antenna or in the dorsal thorax are massively overgrown. In the mid-pupal retina, these clones contain a large excess of inter-ommatidial cells. In the late third instar eye disc, cells in these clones show increased levels of mitosis after (posterior to) the second mitotic wave. Later, at around 25 hours APF, the widespread apotosis seen throughout the developing retina in wild-type and heterozygous cells, is largely suppressed in these clones.

Mer4; exe1 somatic clones in contact with the posterior or lateral margin of the eye fail to produce photoreceptors. Those somatic clones located in the middle of the eye field can produce photoreceptors.

Mer4; exe1 double mutant clones exhibit defects in membrane trafficking of proteins such as N and Egfr.

Df(1)N-54l9 Mer4; exe1 triple transheterozygous mutants suppress the Df(1)N-54l9 heterozygous wing notch phenotype.

ft8/ftG-rv exe1 mutant retinas exhibit an increase in the number of secondary cells per ommatidia (approximately 9, compared to 6 in wild-type), that is not statistically significant from ft8 single mutants.

One copy of exe1 enhances the lethality of ft8/ftG-rv animals. Those that are wild-type for exe1 but mutant for ft8/ftG-rv emerge as 0.32% of the progeny, whereas those that are also mutant for exe1 emerge as 0.269% of the progeny, a small, but statistically significant difference.

exe1;Mer4 double mutants exhibit a large excess of interommatidial cells, in a very similar manner to hpo mutants.

The eye phenotype seen in dshhs.sev.B flies is dominantly enhanced by the addition of exe1 due to an increase in unscorable ommatidia (missing one or more photoreceptors.

Dominantly enhances the head phenotype of Mer3 hemizygotes. Both vein and intervein cells can differentiate in Mer4; exe1 double mutant clones in the wing. Clones that intersect the position of the posterior crossvein disrupt its development. Clones in the position of the anterior crossvein develop normally. Within the mutant intervein and vein clones, apparent defects in proliferation control are seen; in the proximal region of the wing, clonal vein tissue forms a raised protrusion. In other regions of the wing, bulges in the veins are also seen, although more frequently vein clones are merely broadened when compared with the surrounding vein. In the intervein regions, the clonal tissue appears to bulge and crinkle within the confines of the normal tissue, suggesting overproliferation. Cells within the intervein clones appear to differentiate as intervein cells, however, the cuticle deposited at the base of each wing hair within the clone appears to be thickened, and is distinct from cuticle produced by either the surrounding heterozygous intervein or vein cells. Mer4; exe1 double mutant clones in the eye appear to disrupt the progression of the morphogenetic furrow, being seen either as small scars with associated clusters of bristles or as elongated scars and associated indentations running from within the eye field towards the anterior margin. These clones do not differentiate ommatidia. The clones are often associated with overproliferated head cuticle.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

An allelic series can be defined for ex alleles with respect to viability, eclosion rate and penetrance of ex wing phenotype. Going from most to least severe: exe1 >= exl2ey > exe2 > exe6 > ex697 > ex1.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (46)