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General Information
Symbol
Dmel\ApcQ8
Species
D. melanogaster
Name
FlyBase ID
FBal0091898
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
apc1Q8, D-APCQ8, dAPCQ8
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    point mutation
    Nucleotide change:

    C28839483T

    Amino acid change:

    Q427term | Apc-PA; Q427term | Apc-PB; Q427term | Apc-PC

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

    Amino acid replacement: Q426term.

    Nucleotide substitution: C1486T.

    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 ( 1 )
    Modifiers Based on Experimental Evidence ( 1 )
    Disease
    Interaction
    References
    is ameliorated by ewgP1
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In
    Detailed Description
    Statement
    Reference

    ApcQ8 mutant adults display increased number of the progenitor cells (intestinal stem cells, ISCs, and enteroblasts, EBs) as well as aberrant enterocyte (EC) morphology in the midgut, indicating that their cell-to-cell junctions and apico-basal polarity are disrupted, many ECs are also detached from the basement layer forming an abnormal multi-layered epithelium. The excess of progenitor cells in the epithelium is apparent already shortly after eclosion (0-4h), whereas the cell adhesion and epithelium structure defects are not observed yet at this early stage. Notably, no supernumerary adult midgut progenitors are seen in mutant late third instar larvae and the architecture of the larval gut epithelium is also intact.

    Cells in ApcQ8 mutant wing disc clones in third instar larvae do not display any evident morphological defects compared to neighboring cells.

    Posterior midgut ApcQ8 MARCM clones contain significantly more cells and display increased intestinal stem cell proliferation compared to controls.

    Adult-generated ApcQ8, Apc2g10 homozygous double mutant intestinal stem cell clones display hyperplasia 14 days after clone induction compared to control clones.

    ApcQ8 mutant intestinal stem cell clones are similar in size to wild type controls.

    Photoreceptor cells undergo apoptosis in homozygous flies.

    All photoreceptors undergo apoptosis in homozygous ApcQ8 mutants. The pigment cell lattice remains intact. Prior to photoreceptor cell death the photoreceptors appear shorter and aberrant specification of all inner photoreceptors in the dorsal half of the retina to a dorsal rim area fate, as evidenced by enlarged rhabdomeres.

    ApcQ8 adult retina exhibit complete photoreceptor cell loss.

    Mutants show photoreceptor apoptosis.

    All photoreceptors in homozygous mutants undergo apoptosis.

    Ectopic photoreceptor apoptosis is seen in the developing eyes of ApcS76/ApcQ8 pupae, beginning at around 35 hours after puparium formation (APF) and peaking at 42 hours APF. This timing is identical to that of photoreceptor apoptosis occurring at the periphery of the developing eye in wild-type pupae.

    Spindle orientation and centrosome position are perturbed in the germline stem cells of ApcQ8/Df(3R)3450 males.

    Homozygotes survive to adulthood. They show apoptotic death of all retinal neurons in all ommatidia during pupal development. The pigment cell lattice remains intact.

    Asymmetric divisions of neuroblasts appear to be unaffected in the brains of mutant larvae.

    Homozygous adults raised at the permissive temperature are morphologically normal, although they lack pseudopupils. All photoreceptor cells within all ommatidia are missing, although the pigment cell lattice remains intact in newly eclosed flies. The pigment cells enlarge to the point of confluence several days after eclosion. Heterozygous adults have wild-type ommatidia. Retinal axonal projections to the optic lobe are intact in homozygous third instar larvae. At 45-50% pupal development, many apoptotic nuclei are seen in homozygous eye discs. Apoptosis is restricted to the retinal neurons; no apoptotic nuclei are seen in non-neuronal cells in the eye disc. Apoptosis is not seen in wild-type eye discs at this stage. The actin cytoskeleton of the mutant photoreceptor cells is disorganised, in contrast to wild-type.

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

    ApcQ8 has cell lethal | adult stage phenotype, suppressible by ewgP1

    ApcQ8 has cell lethal | adult stage phenotype, suppressible by ewg1/ewg2

    ApcQ8 has size defective | adult stage phenotype, suppressible by ewg1/ewg2

    ApcQ8 has cell lethal | adult stage phenotype, suppressible by ewgP1/ewg2

    ApcQ8 has increased cell death phenotype, suppressible | partially by ninaA[+]/ninaAE110V

    NOT suppressed by
    Statement
    Reference

    Apc2g10, ApcQ8 has increased cell number | somatic clone phenotype, non-suppressible by yki[+]/ykiB5

    Enhancer of
    Statement
    Reference
    NOT Enhancer of
    Other
    Statement
    Reference
    Phenotype Manifest In
    Enhanced by
    NOT Enhanced by
    Suppressed by
    Statement
    Reference

    ApcQ8 has adult midgut epithelium phenotype, suppressible by ewgP1

    ApcQ8 has retina phenotype, suppressible by Df(3L)27-3

    ApcQ8 has retina phenotype, suppressible by Df(3L)ED4196

    ApcQ8 has retina phenotype, suppressible by Df(3L)ED4157

    ApcQ8 has retina phenotype, suppressible | partially by +/Df(3L)ED4136

    ApcQ8 has retina phenotype, suppressible by Df(3L)ED9698

    ApcQ8 has retina phenotype, suppressible by ebd1EY01876/CG3371[+]

    ApcQ8 has retina phenotype, suppressible by ebd1Df5/ebd1240

    ApcQ8 has retina phenotype, suppressible | partially by CG13895190

    ApcQ8 has retina phenotype, suppressible | partially by BacA\p35GMR.PH

    ApcQ8 has photoreceptor | adult stage phenotype, suppressible by ewgP1

    ApcQ8 has photoreceptor | adult stage phenotype, suppressible by ewg1/ewg2

    ApcQ8 has rhabdomere | adult stage phenotype, suppressible by ewg1/ewg2

    ApcQ8 has photoreceptor | adult stage phenotype, suppressible by ewgP1/ewg2

    ApcQ8 has rhabdomere | adult stage phenotype, suppressible | partially by ewgP1/ewg2

    ApcQ8 has photoreceptor cell phenotype, suppressible | partially by ninaA[+]/ninaAE110V

    ApcQ8 has eye photoreceptor cell phenotype, suppressible by Df(3R)w6/+

    ApcQ8 has eye photoreceptor cell phenotype, suppressible | partially by Apc2123/Apc2[+]

    ApcQ8 has eye photoreceptor cell phenotype, suppressible by Apc233

    ApcQ8 has eye photoreceptor cell phenotype, suppressible by Apc245

    ApcQ8 has eye photoreceptor cell phenotype, suppressible by Apc2[+]/Apc233

    ApcQ8 has neuron & retina & pupa phenotype, suppressible | partially by Apc2+t7

    ApcQ8 has eye photoreceptor cell phenotype, suppressible by panciD

    ApcQ8 has eye photoreceptor cell phenotype, suppressible by pan13

    ApcQ8 has eye photoreceptor cell phenotype, suppressible by arm4

    NOT suppressed by
    Statement
    Reference

    Apc2g10, ApcQ8 has axon phenotype, non-suppressible by CLIP-190KO/CLIP-190KO

    ApcQ8 has retina phenotype, non-suppressible by Df(3L)ED4238

    ApcQ8 has retina phenotype, non-suppressible by Df(3L)ED4125

    ApcQ8 has eye photoreceptor cell phenotype, non-suppressible by +/Df(3R)357

    ApcQ8 has eye photoreceptor cell phenotype, non-suppressible by Apc2g10/Apc2[+]

    ApcQ8 has phenotype, non-suppressible by arm8

    Enhancer of
    Statement
    Reference
    NOT Enhancer of
    NOT Suppressor of
    Statement
    Reference

    ApcQ8/Apc2d40 is a non-suppressor of denticle belt | germline clone phenotype of AxnS044230

    Other
    Statement
    Reference

    ApcQ8/Apc[+], Khc8 has phenotype

    Apc2c9/Apc2g10, ApcQ8 has adult midgut | heat sensitive phenotype

    Apc2d40, ApcQ8 has adult head & cuticle | ectopic | somatic clone phenotype

    Apc2d40, ApcQ8 has adult head & cuticle | somatic clone phenotype

    Additional Comments
    Genetic Interactions
    Statement
    Reference

    Apc2N175K, ApcQ8 double homozygous mutant clones (induced using Scer\FLP1SOP.scE1x6) have a failure to prune all ddaC dendrites by 16 h after puparium formation (APF), unlike controls.

    ApcQ8, Apc2g10 homozygous follicle cell clones lead to an increase in the numbers of polar/stalk cells, as compared to controls.

    The adult midgut epithelium defects (increased number of progenitor cells, cell polarity and adhesion defects along with epithelium multi-layering) can be rescued by combination with either ebd1240/Df(3L)ED9698,ebd2136 or with ewgP1 mutant alleles. The increased number of enteroblast cells in midguts of newly eclosed ApcQ8 mutant adults is significantly suppressed by ebd1240 homozygosity.

    Clonal Apc2N175K, ApcQ8 double homozygosity alone or clonal Apc2N175K, ApcQ8 double homozygosity in combination with clonal SxlKK116156 co-expression do not enhance the increased mitotic index in the adult posterior midgut induced by the clonal expression of Ras85DV12.UAS under the control of Scer\GAL4esg-NP7397.

    ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant intestinal stem cell clones in the adult posterior midgut are significantly larger, with more cells, than control wild type clones of similar age, and form multi-layered structures bulging in the lumen of the gut. This phenotype is visible 10 days after clone induction, but becomes more prominent with time. As compared to controls, there is an increase in the number of apoptotic cells in close proximity to the ApcQ8/ApcQ8, Apc2g10/Apc2g10 clones, affecting enterocytes, enteroendocrine cells, and intestinal stem cells. Wild type clones are dramatically smaller and fewer in number in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 clones, as compared to wild type clones in control guts.

    Expression of Diap1Scer\UAS.cHa under the control of Scer\GAL4bun-GSG5961 and Scer\GAL4GSG5966 (along with RU486 to induce expression via the GeneSwitch system) in the gut fully restores growth of wild type clones in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones in the posterior midgut, and suppresses the growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones; however, ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones expressing Diap1Scer\UAS.cHa under the control of Scer\GAL4tub.PU do not have suppressed growth.

    Expression of pucScer\UAS.cMa or bskDN.Scer\UAS under the control of Scer\GAL4bun-GSG5961 and Scer\GAL4GSG5966 (along with RU486 to induce expression via the GeneSwitch system) in the gut fully restores growth of wild type clones in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones in the posterior midgut, and suppresses the growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones. ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones expressing pucScer\UAS.cMa or bskDN.Scer\UAS under the control of Scer\GAL4tub.PU also show suppressed growth. Expression of pucScer\UAS.cMa or bskDN.Scer\UAS in host tissue only, under the control of Scer\GAL4GSG2326, severely suppresses growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones.

    Expression of MycScer\UAS.cZa in host midgut tissue only, under the control of Scer\GAL4GSG2326, fails to suppress the overgrowth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones or the reduced growth of wild type clones.

    hpo42-47/+ or exe1/+, but not ykiB5/+, 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.

    ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones expressing ykiScer\UAS.T:Avic\GFP-EGFP,T:Ivir\HA1 under the control of Scer\GAL4tub.PU do not have suppressed growth.

    Cultured primary neurons derived from doubly homozygous Apc2g10/Apc2g10 ; ApcQ8/ApcQ8 embryos have a significantly increased axon length compared to wild-type controls. This phenotype is unaffected if the embryos are also homozygous for CLIP-190KO.

    Animals maternally and zygotically mutant for both ApcQ8 and Apc2g10 are embryonic lethal, the embryos are smaller and display denticle loss while the naked cuticle is expanded.

    ApcQ8 Apc2g10 double maternal and zygotic mutant embryos exhibit a severe cuticle phenotype characterized by a complete loss of denticles, anterior head holes caused by failure of head involution, and an overall reduction in size caused by increased apoptosis.

    Expression of Apc2WT.T:Avic\GFP-EGFP suppresses the embryonic lethality and cuticle patterning defects seen in maternally and zygotically Apc2g10 ApcQ8 double mutant embryos.

    Expression of Apc2ΔR1R3-R5.T:Avic\GFP-EGFP largely suppresses the embryonic lethality and cuticle patterning defects seen in maternally and zygotically Apc2g10 ApcQ8 double mutant embryos.

    Expression of Apc2Δ15Δ20R1R3-5.T:Avic\GFP-EGFP does not suppress the embryonic lethality and only modestly improves the cuticle patterning defects seen in maternally and zygotically Apc2g10 ApcQ8 double mutant embryos.

    Expression of Apc2Δ15Δ20R1R4-5.T:Avic\GFP-EGFP substantially suppresses the embryonic lethality and cuticle patterning defects seen in maternally and zygotically Apc2g10 ApcQ8 double mutant embryos.

    Apc2g10 ApcQ8 mutant intestinal stem cell clones are significantly larger in size than wild type controls. On day 14 after clone induction the clones begin to develop into multilayered epithelia, and by day 21 many clones have fused with each other, outcompeting the wild type cells to occupy the majority of the midgut. Clone cell polarity appears normal.

    Expression of panΔN.Scer\UAS under the control of Scer\GAL4Act.PU suppresses the increased size of Apc2g10 ApcQ8 mutant intestinal stem cell clones 7 days after clone induction, suppressing the development to hyperplasia. Multilayered clones are rarely observed, even on day 21.

    Expression of pygoKK108114 under the control of Scer\GAL4Act.PU suppresses the increased size of Apc2g10 ApcQ8 mutant intestinal stem cell clones 14 days after clone induction.

    Expression of sggScer\UAS.cUa under the control of Scer\GAL4Act.PU suppresses the increased size of Apc2g10 ApcQ8 mutant intestinal stem cell clones 14 days after clone induction, preventing hyperplasia.

    Expression of EgfrDN.Scer\UAS under the control of Scer\GAL4Act.PU suppresses the increased size of Apc2g10 ApcQ8 mutant intestinal stem cell clones 7 and 14 days after clone induction (ACI). The multilayering phenotype often seen at 21 days ACI is also suppressed.

    Ras85De1B suppresses the increased size of Apc2g10 ApcQ8 mutant intestinal stem cell clones 7 and 14 days after clone induction (ACI). The multilayering phenotype often seen at 21 days ACI is also suppressed. This reduction in cell number is due to reduced proliferation, rather than increased cell death: TUNEL expression is unchanged and expression of the apoptotic protein BacA\p35 has no effect on the phenotype. The remaining increase in clone size seen in the Ras85De1B, Apc2g10, ApcQ8 triple mutant flies is fully suppressed upon expression of panΔN.Scer\UAS under the control of Scer\GAL4Act.PU, and no increase in apoptosis is seen in these flies.

    Flies co-expressing Ras85DV12.Scer\UAS produce fewer intestinal stem cell (ISC) clones per midgut over time compared with Apc2g10 ApcQ8 mutants alone, similar to what is seen when Ras85DV12.Scer\UAS is expressed alone. Approximately 35% of the clones that remain undergo rapid proliferation and develop into large spherical-tumor cell masses (termed 'transformed clones'). There is no obvious increase in apoptosis in these transformed clones and the majority are found in the anterior or posterior midgut rather than the middle midgut. Few enterocytes (ECs) or enteroendocrine cells (ees) are seen, indicating that differentiation is blocked. The remaining 65% of clones are smaller than their wild type counterparts, but the ratio of ISCs to differentiated EC and ee cells is comparable to wild type.

    Approximately 10% of Apc2g10 ApcQ8, Ras85DV12.Scer\UAS mutant ISC clones extrude basally toward the surrounding muscle layer, although the underlying base layer remains unbroken. Expression of Ras85DV12.Scer\UAS induces polarity changes in Apc2g10 ApcQ8 mutant clones.

    Expression of phlScer\UAS.F179 induces cell polarity changes in Apc2g10 ApcQ8 mutant intestinal stem cell clones.

    Expression of hepAct.Scer\UAS under the control of Scer\GAL4Act.PU suppresses the hyperplasia seen in Apc2g10 ApcQ8 mutant intestinal stem cell clones.

    Expression of shgNIG.3722R under the control of Scer\GAL4Act.PU enhances the formation of multicellular epithelia seen in Apc2g10 ApcQ8 double mutant clones. Enterocytes and enteroendocrine cells are both present and the ratio of differentiated cells to progenitor cells is similar to that observed in Apc2g10 ApcQ8 clones alone. The apicobasal polarity of the clone cells is also unaffected.

    23% of embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique) are able to hatch. All of the surviving embryos are maternally double null and zygotically heterozygous for the double-null chromosome. A further 25% of embryos display weak cuticle defects and these are also zygotically heterozygous for Apc2g10 and ApcQ8. All of the maternally and zygotically double mutant embryos die showing severe cuticle defects.

    Expression of Apc2FL.T:Avic\GFP-EGFP partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 46% of embryos are able to hatch. The remaining progeny exhibit a very weak cuticle phenotype.

    Expression of Apc2Δ20RΔB.T:Avic\GFP-EGFP fails to suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 24% of embryos are able to hatch and the severity of the cuticle defects in the remaining progeny is similar to the double mutant alone.

    Expression of Apc2Δ15RΔ20RΔB.T:Avic\GFP-EGFP fails to suppress the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). Between 18% and 24% of embryos are able to hatch, depending on the expression level of the transgenes. The severity of the cuticle defects in the remaining progeny is similar to the double mutant alone.

    Expression of Apc2R3-R5SA.T:Avic\GFP-EGFP partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 68% of embryos are able to hatch.

    Expression of Apc2R3-R5SD.T:Avic\GFP-EGFP partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 40% of embryos are able to hatch.

    Expression of Apc2R1-R5SA.T:Avic\GFP-EGFP partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 51% of embryos are able to hatch. The remaining progeny exhibit a more severe cuticle phenotype than in the double mutant alone.

    Expression of Apc2R1-R5SD.T:Avic\GFP-EGFP partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 49% of embryos are able to hatch. The remaining progeny exhibit a more severe cuticle phenotype than in the double mutant alone.

    Expression of Apc2R1-R5ExR.T:Avic\GFP-EGFP fails to suppress the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 21% of embryos are able to hatch. The severity of the cuticle defects in the remaining progeny is similar to the double mutant alone.

    Expression of Apc2R3-R5ExR.T:Avic\GFP-EGFP partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 50% of embryos are able to hatch. The remaining progeny exhibit a very weak cuticle phenotype.

    Embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones generate naked cuticle. These embryos show approximately 50% lethality (as half the embryos are paternally rescued).

    The cuticle defects of embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones are rescued by expression of Apc2T:Avic\GFP-EGFP,T:Zzzz\Mito-actA. The embryonic lethality is partially rescued (19% lethality is seen).

    The cuticle defects of embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones are strongly rescued by expression of Apc2T:Avic\GFP-EGFP,T:Mmmm\c-Ha-Ras. The embryonic lethality is partially rescued (41% lethality is seen).

    The cuticle defects of embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones are strongly rescued by expression of Apc2T:Myr-Src64B,T:Avic\GFP-EGFP. The embryonic lethality is partially rescued (33% lethality is seen).

    The cuticle defects of embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones are partially rescued by expression of Apc2T:Avic\GFP-EGFP,T:Hsap\CAAX. The embryonic lethality is not rescued.

    The cells around the wing pouch in Apc2g10 ApcQ8 double mutant third instar larval wing disc clones are apically constricted and invaginated.

    No apical constriction is seen in the cells surrounding the wing pouch in ApcQ8 Apc233 double mutant third instar larval clones.

    Apc2g10 ApcQ8 double mutant clone cells generated in the medullar region of third instar larval brains segregate from their neighbours to form cysts. When clones are induced in the medullar neurons the axons do not extend to the medullar neuropil, forming knots in the center of the clones rather than the normal finely fasciculated projections seen in wild type.

    Apc219-3 ApcQ8 double mutant clone cells generated in the medullar region of third instar larval brains segregate from their neighbours to form cysts. When clones are induced in the medullar neurons the axons do not extend to the medullar neuropil, forming knots in the center of the clones rather than the normal finely fasciculated projections seen in wild type.

    Apc219-3 ApcQ8 double mutant clone cells generated in the medullar region of third instar larval brains sometimes segregate from their neighbours to form cysts. When clones are induced in the medullar neurons the axons extend correctly to the medullar neuropil.

    ApcQ8 enhances the embryonic cuticle phenotype seen in Apc2g10 mutants. In Apc2g10 ApcQ8 double mutant embryos all cells are converted to posterior fates. No cells are seen that secrete the denticles normally seen in the anterior cuticle.

    Expression of Apc2ΔArmRepeats.T:Avic\GFP-EGFP provides a very weak rescue of the anterior fate loss seen in Apc2g10 ApcQ8 maternal/zygotic mutant embryos.

    Expression of Apc2T:Avic\GFP-EGFP rescues the anterior fate loss seen in Apc2g10 ApcQ8 maternal/zygotic mutant embryos.

    Apc219-3 ApcQ8 AxnS044230 triple mutant clone cells generated in the medullar region of third instar larval brains sometimes segregate from their neighbours to form cysts. When clones are induced in the medullar neurons the axons extend correctly to the medullar neuropil.

    ebd1240/ebd1Df5 suppresses the apoptosis of photoreceptor cells which is seen in ApcQ8 homozygotes, such that the rescued photoreceptors are wild type in length.

    Homozygosity for CG13895190 partially suppresses the apoptosis of photoreceptor cells which is seen in ApcQ8 homozygotes; photoreceptors are seen only in a subset of ommatidia, and these ommatidia have less than seven photoreceptors.

    ebd2136 weakly suppresses the apoptosis of photoreceptor cells which is seen in ApcQ8 homozygotes.

    ebd1QF1 suppresses the photoreceptor apoptosis phenotype seen in ApcQ8 flies.

    The photoreceptor apoptosis phenotype seen in ApcQ8 flies is suppressed by Df(3L)27-3/Df(3L)ED4136.

    Embryos maternally and zygotically double mutant for ApcQ8 and Apc2N175K display a naked cuticle phenotype.

    Embryos maternally and zygotically double mutant for ApcQ8 and Apc2f90 display a naked cuticle phenotype.

    Expression of AxnScer\UAS.T:Avic\GFP under the control of Scer\GAL4arm.PS restores normal-looking denticle belts in embryos maternally and zygotically mutant for ApcQ8 and Apc2N175K.

    Expression of AxnScer\UAS.T:Avic\GFP under the control of Scer\GAL4arm.PS is unable to restore normal-looking denticle belts in embryos that are maternally and zygotically mutant for ApcQ8 and Apc2f90. Every single embryo exhibits a completely naked cuticle, without any sign of denticle restoration.

    Expression of AxnScer\UAS.T:Avic\GFP under the control of Scer\GAL4arm.PS restores normal-looking denticle belts in embryos derived from females containing ApcQ8 Apc2f90 double mutant germline clones crossed with wild type males.

    Expressing AxnFGmut.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4arm.PS does not suppress the naked cuticle phenotype seen in ApcQ8 Apc2f90 double mutant embryos. Only occasional individual denticles are seen.

    Embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones generate naked cuticle. These embryos show approximately 50% lethality (as half the embryos are paternally rescued).

    The cuticle defects and lethality of embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones are rescued by expression of Apc2WT.T:Avic\GFP-EGFP, Apc2ΔR3.T:Avic\GFP-EGFP or Apc2Δ15.T:Avic\GFP-EGFP.

    The cuticle defects and lethality of embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones are not rescued by Apc2KeepR3.T:Avic\GFP-EGFP, Apc2Δ20.T:Avic\GFP-EGFP, Apc2ΔR2.T:Avic\GFP-EGFP, Apc2ΔB.T:Avic\GFP-EGFP or Apc2d40.T:Avic\GFP-EGFP.

    Apc2Δ15Δ20.T:Avic\GFP-EGFP does not rescue the cuticle defects of embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones. Apc2Δ15Δ20.T:Avic\GFP-EGFP may show some dominant negative activity, as 82% embryonic lethality is seen, suggesting that the ability of paternally supplied Apc[+] and Apc2[+] to rescue embryonic lethality is compromised.

    Apc2ΔSAMP.T:Avic\GFP-EGFP does not rescue the cuticle defects of embryos derived from Apc2g10 ApcQ8 males crossed to females containing double homozygous germline clones. Apc2ΔSAMP.T:Avic\GFP-EGFP may show some dominant negative activity, as 71% embryonic lethality is seen, suggesting that the ability of paternally supplied Apc[+] and Apc2[+] to rescue embryonic lethality is compromised.

    Hemizygous ewgP1 suppresses the apoptosis seen in ApcQ8 mutant photoreceptors. This apoptosis can be restored by expressing ewgelav.NS.

    Hemizygous ewg1/ewg2 suppresses the apoptosis seen in ApcQ8 mutant photoreceptors. The shortening of photoreceptor length seen prior to apoptosis is also suppressed, as is the rhabdomere enlargement seen as a result of misspecification of all of the photoreceptors in the dorsal half of the retina to a dorsal rim area fate.

    Hemizygous ewgP1/ewg2 suppresses the apoptosis seen in ApcQ8 mutant photoreceptors. The shortening of photoreceptor length seen prior to apoptosis is also suppressed, and the rhabdomere enlargement seen as a result of misspecification of all of the photoreceptors in the dorsal half of the retina to a dorsal rim area fate is also partially suppressed. This is most evident near the dorsal-ventral equator.

    23% of embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique) are able to hatch. All of the surviving embryos are maternally double null and zygotically heterozygous for the double-null chromosome, whilst all of the maternally and zygotically mutant embryos died. The embryos display a range of cuticle defects including a reduction in cuticle size due to excess cell death, a hole in the anterior cuticle due to a failure in head involution and the production of excess smooth cuticle at the expense of denticles.

    Expression of Apc2FL.T:Avic\GFP-EGFP suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 46% of embryos are able to hatch. The cuticle defects are also significantly rescued.

    Expression of Apc2ΔC30.T:Avic\GFP-EGFP suppresses the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 46% of embryos are able to hatch. The cuticle defects are also significantly rescued.

    Expression of Apc2N-SAMP.T:Avic\GFP-EGFP is unable to suppress the lethality seen in embryos derived from females carrying homozygous Apc2g10 ApcQ8 germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 17% of embryos are able to hatch and the severity of the cuticle defects is similar to in the double mutant alone.

    Apc2g10, ApcQ8/Apc2c9 adults shifted to the non-permissive temperature show an increase in BrdU incorporation in the midgut compared to controls maintained at the permissive temperature.

    5 days after clone induction in adults, Apc2g10, ApcQ8 double mutant clones in the midgut have a significantly increased number of cells per clone compared to controls. There is a significant increase in cell size both in the anterior and posterior midgut, with the average size being greater in the posterior midgut. Intestinal stem cell self-renewal is unaffected at 5 and 10 days after clone induction in the adult.

    20 days after clone induction in adults, midguts containing Apc2g10, ApcQ8 double mutant clones are associated with gross anatomical changes, including hyperplasia and multilayered cellular masses that distort the luminal surface of the midgut.

    Apc2g10, ApcQ8 double mutant clones in the adult midgut that are also expressing NdsRNA.P.Scer\UAS under the control of Scer\GAL4tub often show extensive proliferation and multilayering 10 days after induction in the adult. The number of intestinal stem cells present and the mitotic index of the intestinal stem cells 5 days after induction is significantly higher in Apc2g10, ApcQ8 double mutant clones in the adult midgut that are also expressing NdsRNA.P.Scer\UAS under the control of Scer\GAL4tub compared to clones expressing NdsRNA.P.Scer\UAS under the control of Scer\GAL4tub in an otherwise wild-type background.

    Apc233 ApcQ8 double mutant intestinal stem cell clones in the adult midgut show hyperplasia.

    The hyperplasia seen in Apc233 ApcQ8 double mutant intestinal stem cell clones in the adult midgut is completely suppressed if they are also expressing panΔN.Scer\UAS under the control of Scer\GAL4tub.

    The hyperplasia seen in Apc2g10 ApcQ8 double mutant intestinal stem cell clones in the adult midgut is partially suppressed if they are also expressing panΔN.Scer\UAS under the control of Scer\GAL4tub.

    A heterozygous or homozygous ninaAE110V background is sufficient to induce a partial rescue of photoreceptor cells from ApcQ8-induced loss.

    The ventral cuticle of ApcQ8, Apc2d40 double mutant embryos is naked.

    Expression of AxnScer\UAS.cHa under the control of Scer\GAL4da.G32 blocks the naked-cuticle phenotype of ApcQ8, Apc2d40 double mutant embryos.

    Expression of AxnScer\UAS.T:Src64B,T:Zzzz\FLAG under the control of Scer\GAL4da.G32 has no effect on the naked-cuticle phenotype of ApcQ8, Apc2d40 double mutant embryos.

    Expression of Apc2Scer\UAS.T:Avic\GFP under the control of Scer\GAL4da.G32 restores wild-type patterning of the ventral cuticle in ApcQ8, Apc2d40 double mutant embryos.

    Expression of Apc2Scer\UAS.T:Src64B,T:Zzzz\FLAG under the control of Scer\GAL4da.G32 fails to restore wild-type patterning of the ventral cuticle in ApcQ8, Apc2d40 double mutant embryos.

    Triple mutants for AxnS044230, ApcQ8 and Apc2d40 have naked ventral embryonic epidermis.

    The ventral denticle belt phenotype of AxnS044230, ApcQ8, Apc2d40 triple mutants is suppressed by expression of AxnScer\UAS.cHa under the control of Scer\GAL4da.G32.

    Expression of AxnScer\UAS.T:Src64B,T:Zzzz\FLAG under the control of Scer\GAL4da.G32 has no effect on the ventral denticle belt phenotype of AxnS044230, ApcQ8, Apc2d40 triple mutants.

    Expression of Apc2Scer\UAS.T:Avic\GFP under the control of Scer\GAL4da.G32 has no effect on the ventral denticle belt phenotype of AxnS044230, ApcQ8, Apc2d40 triple mutants.

    Expression of Apc2Scer\UAS.T:Src64B,T:Zzzz\FLAG under the control of Scer\GAL4da.G32 has no effect on the ventral denticle belt phenotype of AxnS044230, ApcQ8, Apc2d40 triple mutants.

    ApcQ8 Apc25-3/ApcQ8 Apc233 double mutants show expansion of sternal territory in the abdomen and ectopic sternal bristles, at the expense of the pleura.

    ApcQ8 Apc2G5028/ApcQ8 Apc233 double mutants show expansion of sternal territory in the abdomen and ectopic sternal bristles, at the expense of the pleura.

    ApcQ8 Apc25-3 double homozygotes show loss of sternites and sternal bristles and expansion of the pleura in the abdomen.

    ApcQ8 Apc25-3/ApcQ8 Apc2G5028 double mutants show loss of sternites and sternal bristles and expansion of the pleura in the abdomen.

    ApcQ8 Apc25-3/ApcQ8 Apc219-3 double mutants show a wing to notum transformation.

    The photoreceptor cell apoptosis phenotype seen in ApcQ8 homozygotes is suppressed by Apc233/+ but not by Apc2g10/+.

    There is no difference in the frequency of mispositioned oocytes between wild type and Apc2g10, ApcQ8 double mutant mutant germlines.

    Apc2g10, ApcQ8 maternal/zygotic double mutant embryos show no defects in epithelial structure and do not show a total disruption of the cuticle.

    Apc2g10, ApcQ8 maternally mutant syncytial embryos show similar levels (35 vs 37%) of cortical nuclei movement to the anterior to Apc2g10 syncytial embryos.

    Apc2g10, ApcQ8 maternally mutant syncytial embryos do not have significant defects in overall spindle morphology or orientation but do show a slight but significant lengthening of the pole-to-pole distance. These double mutants show normal symmetric cell division.

    Ectopic photoreceptor apoptosis in the developing eyes of ApcS76/ApcQ8 pupae is greatly reduced by Df(3L)H99/+.

    ApcQ8, Apc2N175K double mutant embryos have a naked cuticle phenotype.

    ApcQ8 Apc2d40 double mutant homozygotes derived from heterozygous parents differentiate a normal larval cuticle but die during the larval stage. ApcQ8 Apc2d40 double mutant clones in the wing autonomously form marginal structures, adopting the fate of those marginal cells that are closest to the clone; they form bristles in the anterior and thin tapered hairs in the posterior. The clones can occupy up to 1/3 of the wing surface. ApcQ8 Apc2d40 double mutant clones result in outgrowths in the proximal leg and duplications in the distal leg. The duplications arise from the dorsal side of the leg and contain both homozygous clone cells and neighbouring heterozygous cells. Double mutant clones are rarely found in parts of the leg that have differentiated into dorsal structures. Double mutant clones are frequently found in ventral structures and ventral bristles in these clones are often morphologically normal. ApcQ8 Apc2d40 double mutant clones in the eye show transformation into ectopic head cuticle. These clones can occupy up to half the eye. ApcQ8 Apc2d40 double mutant clones also produce mutant phenotypes in the head cuticle, antennae, labial disc derivatives, notum, tergites and genitalia. The expansion of naked cuticle seen in embryos derived from Apc2d40 females mated to Apc2d40 males is enhanced if the maternal or zygotic dose of Apc is reduced by half (using ApcQ8); in these double mutant embryos most denticles are eliminated. Embryos derived from ApcQ8 Apc2d40 double mutant germline clones (lacking maternal but not zygotic Apc and Apc2) have some cuticle defects but often hatch and survive to adulthood. Animals derived from ApcQ8 Apc2d40 double mutant germline clones and also lacking zygotic Apc (animal is homozygous for ApcQ8) die either during embryonic or larval stages and differentiate partially naked cuticles. The cuticle defects of embryos derived from ApcQ8 Apc2d40 double mutant germline clones are also enhanced if the embryos lack zygotic Apc2 (embryo is homozygous for Apc2d40). One copy of Apc2+t7 is able to partially prevent the apoptosis of retinal neurons seen in ApcQ8 homozygotes.

    Apc2d40, ApcQ8 double homozygotes die a first instar larvae. Apc2g10, ApcQ8 double homozygotes die as second instar larvae. Apc2ΔS, ApcQ8 double homozygotes die as second instar larvae. Double mutant second larval instar brains are essentially normal in size and the optic anlage has become epithelial. Second instar larval mushroom body neuroblasts proliferate as normal, but the number of other mitotic neuroblasts is drastically reduced relative to wild type. BrdU incorporation in the brain is drastically reduced in second instar larvae, with most labelled cells appearing to be mushroom body neuroblasts. The remaining larval neuroblasts retain the ability to divide asymetrically. The axonal scaffold is unaltered in Apc2ΔS, ApcQ8 double mutant embryos.

    Apc2d40 ApcQ8, Apc2ΔS ApcQ8, and Apc2g10 ApcQ8 double zygotic mutants are embryonic viable and exhibit a wild-type cuticle pattern, but die as larvae. In the embryonic progeny of Apc2ΔS ApcQ8/Apc2ΔS males and females crossed to each other ventral cells secrete only naked cuticle. This is a more severe cuticle phenotype than that seen in Apc2ΔS maternal and zygotic mutant embryos. Apc2d40 ApcQ8 maternal and zygotic double mutants exhibit a much stronger embryonic cuticle phenotype than Apc2d40 maternal and zygotic single mutants. Maternal and zygotic double mutant cuticles are shorter, and, unlike Apc2d40 maternal and zygotic single mutants, most embryos completely lack denticles. Maternal and zygotic double mutants also exhibit a complete failure of head involution. Dorsally, all cells are transformed to the fate normally adopted by posterior cells, and thus all secrete fine dorsal hairs. These embryos also exhibit slight abnormalities in dorsal closure not seen in the single mutant. Embryos receiving paternal wild-type copies of Apc2 and Apc are rescued to viability. Patches of ectopic wing margin bristles are seen in the wing blades of animals in which Apc2d40 ApcQ8 double mutant clones have been induced. Ectopic bristles are also seen in the nota of these animals.

    The penetrance of the oocyte mislocalisation phenotype see in Apc2N175K mutant females is increased to 32% if they are also mutant for ApcQ8.

    Overexpression of BacA\p35GMR.PH in ApcQ8 homozygotes rescues the retinal neurons from death. The rescued photoreceptors appear normal at the apical surface of the eye, but at more basal levels they have dramatically shrunken diameters and lose contacts with their neighbours. Many photoreceptors are rescued from death in homozygotes carrying one copy of arm4. The rescued photoreceptors appear completely normal from apex to base. Many photoreceptors are rescued from death in ApcQ8 homozygotes carrying one copy of armS5.T:Hsap\MYC, armS12.T:Hsap\MYC or armS15.T:Hsap\MYC in an arm4/+ background. Many photoreceptors are rescued from death in ApcQ8 homozygotes carrying one copy of sggScer\UAS.cSa expressed under the control of Scer\GAL4elav-C155. The rescued cells are only seen at the apical surface of the eye, there is no rescue more basally. Some photoreceptors are rescued from death in ApcQ8 homozygotes carrying one copy of panciD or pan13. The rescued cells are only seen at the apical surface of the eye, there is no rescue more basally. Photoreceptors are not rescued from death in ApcQ8 homozygotes carrying one copy of armS14.T:Hsap\MYC in an arm4/+ background. Photoreceptors are not rescued from death in homozygotes carrying one copy of arm8.

    Xenogenetic Interactions
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    Expression of BacA\p35Scer\UAS.cUa under the control of Scer\GAL4bun-GSG5961 and Scer\GAL4GSG5966 (along with RU486 to induce expression via the GeneSwitch system) in the gut fully restores growth of wild type clones in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones in the posterior midgut, and suppresses the growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones; however, ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones expressing BacA\p35Scer\UAS.cUa under the control of Scer\GAL4tub.PU do not have suppressed growth.

    BacA\p35GMR.PH ApcQ8 flies have shortened photoreceptors, which are visible in apical cross sections of the retina, but do not extend to its base.

    Complementation and Rescue Data
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