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Allele Dmel\exe1
| General Information | |||
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| Symbol | Dmel\exe1 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0031224 | |
| Feature type | allele | Associated gene | Dmel\ex |
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| Allele class | loss of function allele, amorphic allele - genetic evidence | ||
| Mutagen | P-element activity | ||
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
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Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References deletion evidence=experimental linked_to=HindIII-HindIII_rfrag 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 | |||
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
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| Progenitor genotype | |||
| Nature of the lesion | Statement Reference Small deletion that removes the 5' end of ex. Small deletion that removes 3-12kb of genomic DNA, including the first ex exon. | ||
| Caused by insertion | |||
| Cytology | |||
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Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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Detailed Description
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Statement Reference Cells in homozygous clones in the wing disc accumulate F-actin near the apical surface. ex[e1] 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 ex[e1] (generated using the eyFLP method without cell lethal) show mild overgrowth compared to controls. Pupal retinae composed of homozygous ex[e1] mutant cells show an increase in the number of interommatidial cells. ex[e1] 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. ex[e1] 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. | |||
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External Data
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Interactions
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Phenotypic Class
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| Enhanced by | |||
Statement Reference | |||
| Suppressed by | |||
Statement Reference | |||
| NOT suppressed by | |||
Statement Reference | |||
| Enhancer of | |||
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| Other | |||
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Phenotype Manifest In
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| Enhanced by | |||
Statement Reference | |||
| NOT Enhanced by | |||
Statement Reference exe1 has phenotype, non-enhanceable by Rac1V12.hs.sev exe1 has phenotype, non-enhanceable by Rho1V14.sev | |||
| Suppressed by | |||
Statement Reference | |||
| NOT suppressed by | |||
Statement Reference exe1 has phenotype, non-suppressible by Rac1V12.hs.sev exe1 has phenotype, non-suppressible by Rho1V14.sev | |||
| Enhancer of | |||
Statement Reference | |||
| NOT Enhancer of | |||
Statement Reference exe1 is a non-enhancer of phenotype of Rac1V12.hs.sev exe1 is a non-enhancer of phenotype of Rho1V14.sev | |||
| NOT Suppressor of | |||
Statement Reference exe1 is a non-suppressor of phenotype of Rac1V12.hs.sev exe1 is a non-suppressor of phenotype of Rho1V14.sev | |||
| Other | |||
Statement Reference | |||
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Additional Comments
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Genetic Interactions
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Statement Reference Wings from pyd[ex147]/pyd[tam] flies are broader compared to control wings, and this phenotype is enhanced in a ex[e1]/+ background. Expression of yki[NIG.4005R] under the control of Scer\GAL4[unspecified] in ex[e1] 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 ex[e1]/ex[e1] and kibra[1]/kibra[3] (clones induced using the eyFLP method without cell lethal) do not eclose and normal head structures are displaced by overgrown tissue.
ex[e1] kibra[1] double mutant clones in the eye imaginal disc are very large and invariably adopt a rounded shape. Pupal retinae composed of crb[82-04] ex[e1] double mutant cells show a similar number of interommatidial cells as do the single mutants. ex[e1] ; kibra[del] 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. dm[Scer\UAS.cZa] overexpression clones (under the control of Scer\GAL4[hh.PU]) found in the posterior of the wing disc strongly enhance the proliferative activity of ex[e1] mutant cells. In addition these cells are larger in dm[Scer\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). Somatic clones homozygous for Mer[4] and ex[e1] 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. 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. | |||
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Xenogenetic Interactions
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Complementation & Rescue Data
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Stocks
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Notes on Origin
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 External Crossreferences & Linkouts
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Synonyms & Secondary IDs
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| Reported As | |||
| Symbol Synonym | exe1 (Polesello et al., 2006, Tyler et al., 2007, Maitra et al., 2006, Silva et al., 2006, Bennett and Harvey, 2006, Fletcher et al., 2012, Baumgartner et al., 2010, Fernández et al., 2011, Polesello et al., 2006, Silva, 2006, Hamaratoglu et al., 2006, Oh and Irvine, 2008, Willecke et al., 2006, Sun et al., 2008, Genevet et al., 2009, Yu et al., 2010, Yu et al., 2010, Baumgartner et al., 2010, Genevet et al., 2010, Pellock et al., 2007, Ziosi et al., 2010, Ling et al., 2010, Djiane et al., 2011, Grusche et al., 2011, Cho et al., 2006) | ||
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References
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Recent research papers ( 5 ) | |||
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