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General Information
Symbol
Dmel\Apc2g10
Species
D. melanogaster
Name
FlyBase ID
FBal0141947
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
point mutation
Reported amino acid change:

S383term

Comment:

A change in two nucleotides is required for a S383@ mutation relative to the sequenced strain.

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

Amino acid replacement: S383term.

Premature stop codon in Arm repeat.

Amino acid replacement: ??term.

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

Nearly all Apc2g10/Apc2g10 embryos from Apc2g10 homozygous parents fail to hatch. Progeny of Apc2g10/+ parents show rare embryonic mortality and no visible cuticle defects in embryos that fail to hatch; the proportion of homozygous adult progeny is reduced compared to the expected Mendelian proportion.

Apc2g10 maternal and zygotic mutant embryos exhibit a moderate cuticle phenotype characterized by a few remaining denticles, some anterior defects and a moderate reduction in size caused by increased apoptosis.

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

Apc2g10 mutant intestinal stem cell clones are similar in size to wild type controls.

Embryos that are both maternal and zygotic mutant for Apc2g10 (generated using the FRT-FLP-DFS technique) exhibit complete lethality. 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.

Most cells secrete only naked cuticle in homozygous embryos derived from homozygous females.

Homozygous embryos derived from homozygous females show 96% lethality at the embryonic stage.

In maternal/zygotic Apc2g10 mutant embryos almost all cells are converted to posterior fates, with only a few cells secreting the denticles normally seen in anterior cells. 96% of lethality occurs at the embryonic stage.

83% of Apc2g10 mutants expressing Apc2ΔArmRepeats.T:Avic\GFP-EGFP are lethal at the embryonic stage. Adult escapers are seen.

86% of Apc2g10 mutants expressing Apc2Armrepeatsonly.T:Avic\GFP-EGFP are lethal at the embryonic stage. No adult escapers are seen.

Homozygous embryos derived from homozygous females show 96% lethality at the embryonic stage.

Embryos that are both maternal and zygotic mutant for Apc2g10 (generated using the FRT-FLP-DFS technique) exhibit complete lethality. 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. Defects in pseudocleavage furrow extension are also seen, with 66% of syncytial blastoderm stage embryos forming incomplete cortical actin rings in the four divisions before cellularisation.

Embryos maternally mutant for Apc2g10 exhibit incomplete actin rings at a significantly higher frequency than wild-type ones. The incomplete actin rings are occasionally associated with apparent spindle collisions. Although actin pseudocleavage furrows initiate in some of these embryos, they do not extend normally.

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

35% of Apc2g10 maternally mutant syncytial embryos show movement of over 2% of cortical nuclei into the embryo interior, compared to 0-3% of wild-type embryos. The mutant embryos also show compromised actin furrows. 7% of the progeny from Apc2g10/+ mothers also show the nuclear retention phenotype.

The cuticle of an average Apc2g41 maternal/zygotic embryo shows an anterior hole, is 50-60% the length of wild-type and has at most 2 patches of denticles remaining.

Asymmetric division of neuroblasts appears to be unaffected in the brains of Apc2g10/Apc2f90 larvae. Apc2g10 has a more severe maternal effect embryonic phentype than either Apc2ΔS or Apc2d40.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference

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

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

Apc2g10/Apc2[+], bratDG19310/brat11 has type II neuroblast | supernumerary phenotype, suppressible | partially by arm8/arm[+]

NOT suppressed by
Statement
Reference

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

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

Apc2g10/Apc2[+] is a non-suppressor of eye photoreceptor cell phenotype of ApcQ8

Other
Statement
Reference

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

Additional Comments
Genetic Interactions
Statement
Reference

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

ApepPEY02585 homozygous or heterozygous progeny from ApepPEY02585 heterozygous parents do not reach adulthood when also homozygous for Apc2g10, inherited from heterozygous parents.

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.

ApcWT.T:Avic\GFP, ApcendsatSAMP.T:Avic\GFP and Apc::Apc2APC2+APC1CT.T:Avic\GFP each strongly rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). The embryonic lethality is also partially rescued (31%, 28% and 21% lethality is seen respectively) and viable adults are recovered.

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

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.

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.

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.

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.

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.

Apical actin in the offspring of Eb1B13/+; Apc2g10 mothers appears normal. Furthermore, there is no significant increase in the percentage of incomplete actin rings in these embryos as compared to wild-type.

Embryos in the offspring of diak07135/+ ; Apc2g10 mothers have increased metaphase cap-like actin at the apical surface as compared to single heterozygous controls. The number of incomplete rings is significantly increased in these embryos.

The photoreceptor cell apoptosis phenotype seen in ApcQ8 homozygotes is not suppressed 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.

Apc2g10, ApcQ8 double homozygotes die as second instar larvae.

Apc2g10 ApcQ8 double zygotic mutants are embryonic viable and exhibit a wild-type cuticle pattern, but die as larvae.

Xenogenetic Interactions
Statement
Reference

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.

Complementation and Rescue Data
Partially rescued by

Apc2g10 is partially rescued by Apc2AA

Apc2g10 is partially rescued by Apc2Δ20.EGFP

Apc2g10 is partially rescued by Apc2Δ15.EGFP

Apc2g10 is partially rescued by Apc2ΔR2.EGFP

Apc2g10 is partially rescued by Apc2ΔB.EGFP

Apc2g10 is partially rescued by Apc2FL.EGFP

Apc2g10 is partially rescued by Apc2N-SAMP.EGFP

Apc2g10 is partially rescued by Apc2ΔC30.EGFP

Apc2g10 is partially rescued by Apc2cMa

Apc2g10 is partially rescued by Apc2cMa

Not rescued by
Comments

The embryonic lethality along with the cuticle defects (loss of denticles, expansion of naked cuticle) characteristic for maternal/zygotic Apc2g10,ApcQ8 mutants is rescued by combination with Apc2WT.T:Avic\GFP-EGFP.

Expression of Apc2WT.T:Avic\GFP-EGFP rescues the embryonic lethality and cuticle patterning defects seen in maternally and zygotically Apc2g10 mutant embryos. The rescued stock is adult viable.

Expression of Apc2ΔR1R3-R5.T:Avic\GFP-EGFP largely rescues the embryonic lethality and cuticle patterning defects seen in maternally and zygotically Apc2g10 mutant embryos. The rescued stock is adult viable.

Expression of Apc2Δ15Δ20R1R3-5.T:Avic\GFP-EGFP substantially rescues the embryonic lethality and cuticle patterning defects seen in maternally and zygotically Apc2g10 mutant embryos.

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

Expression of Apc2FL.T:Avic\GFP-EGFP completely rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 98% hatch rate. Very weak cuticle defects are seen in the few embryos that fail to hatch.

Expression of Apc2Δ20RΔB.T:Avic\GFP-EGFP partially rescues the lethality and cuticle phenotypes seen in embryos that are both maternally and zygotically mutant for Apc2g10. The level of rescue is dependent on the expression levels of the transgenes, with higher expression significantly reducing the degree of rescue.

Expression of Apc2Δ15RΔ20RΔB.T:Avic\GFP-EGFP partially rescues the lethality and cuticle phenotypes seen in embryos that are both maternally and zygotically mutant for Apc2g10. The level of rescue is dependent on the expression levels of the transgenes, with higher expression significantly reducing the degree of rescue.

Expression of Apc2R3-R5SA.T:Avic\GFP-EGFP significantly rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 93% hatch rate. Weak cuticle defects are seen in the few embryos that fail to hatch.

Expression of Apc2R3-R5SD.T:Avic\GFP-EGFP significantly rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 97% hatch rate. Weak cuticle defects are seen in the few embryos that fail to hatch.

Expression of Apc2R1-R5SA.T:Avic\GFP-EGFP partially rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 72% hatch rate. Very weak cuticle defects are seen in the embryos that fail to hatch.

Expression of Apc2R1-R5SD.T:Avic\GFP-EGFP partially rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 89% hatch rate. Very weak cuticle defects are seen in the embryos that fail to hatch.

Expression of Apc2R1-R5ExR.T:Avic\GFP-EGFP modestly rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 34% hatch rate. Weak cuticle defects are seen in the embryos that fail to hatch.

Expression of Apc2R3-R5ExR.T:Avic\GFP-EGFP partially rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 91% hatch rate. Weak cuticle defects are seen in the embryos that fail to hatch.

Apc2T:Avic\GFP-EGFP,T:Zzzz\Mito-actA rescues the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). The embryonic lethality of these Apc2 mutants is largely rescued (14% embryonic lethality is seen), and viable adults are obtained.

Apc2T:Avic\GFP-EGFP,T:Mmmm\c-Ha-Ras and Apc2T:Myr-Src64B,T:Avic\GFP-EGFP each rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). The embryonic lethality of these Apc2 mutants is partially rescued (34% and 23% embryonic lethality is seen respectively), and viable adults are obtained.

Apc2T:Avic\GFP-EGFP,T:Hsap\CAAX partially rescues the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). The embryonic lethality of these Apc2 mutants is not rescued.

Expression of Apc2ΔArmRepeats.T:Avic\GFP-EGFP partially rescues the loss of anterior fates seen in maternal/zygotic Apc2g10 mutant embryos. Denticle belts are largely restored to the cuticle.

Expression of Apc2Armrepeatsonly.T:Avic\GFP-EGFP partially rescues the loss of anterior fates seen in maternal/zygotic Apc2g10 mutant embryos.

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

Apc2WT.T:Avic\GFP-EGFP and Apc2ΔR3.T:Avic\GFP-EGFP each rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). The embryonic lethality of these Apc2 mutants is also rescued, to adult viability.

Apc2ΔR1R4-R5.T:Avic\GFP-EGFP, Apc2ΔR3-R5.T:Avic\GFP-EGFP, Apc2Δ15.T:Avic\GFP-EGFP, Apc2ΔR2.T:Avic\GFP-EGFP and Apc2ΔB.T:Avic\GFP-EGFP each rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). The embryonic lethality of these Apc2 mutants is partially rescued (41%, 44%, 53%, 43% and 46% embryonic lethality is seen respectively), and viable adults are obtained.

Apc2KeepR3.T:Avic\GFP-EGFP and Apc2Δ20.T:Avic\GFP-EGFP each significantly rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). The embryonic lethality of these Apc2 mutants is not rescued.

Apc2d40.T:Avic\GFP-EGFP, Apc2ΔSAMP.T:Avic\GFP-EGFP and Apc2EndatB.T:Avic\GFP-EGFP each have some limited residual ability to rescue the cuticle defects and lethality of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). No adults are recovered.

Apc2Δ15Δ20.T:Avic\GFP-EGFP fails to rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2g10 embryos derived from Apc2g10 females). The embryonic lethality of these Apc2 mutants is also not rescued.

Expression of Apc2FL.T:Avic\GFP-EGFP completely rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 96% hatch rate and a viable, fertile stock.

Expression of Apc2N-SAMP.T:Avic\GFP-EGFP partially rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2g10, resulting in a 68% hatch rate. Fewer embryonic cuticle defects are also seen.

Expression of Apc2ΔC30.T:Avic\GFP-EGFP completely rescues the lethality seen in embryos that are maternally and zygotically mutant for Apc2g10, resulting in a viable, fertile stock.

Expression of Apc2FL.T:Avic\GFP-EGFP significantly rescues the pseudocleavage furrow extension defects seen in embryos that are both maternally and zygotically mutant for Apc2g10 (generated using the FRT-FLP-DFS technique). 7% of cortical actin rings in the four cortical divisions before cellularisation are incomplete.

Expression of Apc2ΔC30.T:Avic\GFP-EGFP partially rescues the pseudocleavage furrow extension defects seen in embryos that are both maternally and zygotically mutant for Apc2g10 (generated using the FRT-FLP-DFS technique). 38% of cortical actin rings in the four cortical divisions before cellularisation are incomplete.

Expression of Apc2N-SAMP.T:Avic\GFP-EGFP partially rescues the pseudocleavage furrow extension defects seen in embryos that are both maternally and zygotically mutant for Apc2g10 (generated using the FRT-FLP-DFS technique). 41% of cortical actin rings in the four cortical divisions before cellularisation are incomplete.

Expression of the Apc2cMa transgene partially rescues the nuclear retention phenotype of Apc2g10 syncytial embryos - the penetrance of the phenotype falls from 35% to only 14% in rescued embryos.

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Apc2 alleles can be divided into three categories based on their embryonic cuticle phenotypes, from weak to moderate to strong: Apc2e90 = Apc2b5 = Apc2N175K < Apc2c9 = Apc2ΔS = Apc2d40 < Apc2g41 = Apc2f90 = Apc2g10.

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