Allele Dmel\Apc2^g10

General Information
Symbol	Dmel\Apc2^g10	Species	D. melanogaster
Name		FlyBase ID	FBal0141947
Feature type	allele	Associated gene	Dmel\Apc2

Allele class	amorphic allele - genetic evidence, loss of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (McCartney et al., 2006) loss of function allele (Akong et al., 2002)
Mutagen	ethyl methanesulfonate (Akong et al., 2002, Akong et al., 2002, McCartney et al., 2006)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Amino acid replacement: S383@. (McCartney et al., 2006) Amino acid replacement: ??@. Stop codon in Arm repeat. (Akong et al., 2002)
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| embryonic stage (Roberts et al., 2012, Roberts et al., 2011, Roberts et al., 2012) lethal \| embryonic stage (with Apc2^{Armrepeatsonly.T:Avic\GFP-EGFP}) (Roberts et al., 2012) lethal \| embryonic stage \| germline clone (Zhou et al., 2011, Kunttas-Tatli et al., 2012) lethal \| embryonic stage \| rescuable maternal effect (McCartney et al., 2006) partially lethal - majority live \| embryonic stage (with Apc2^{ΔArmRepeats.T:Avic\GFP-EGFP}) (Roberts et al., 2012) viable (Akong et al., 2002)
Phenotype Manifest In
	actin filament \| embryonic stage 4 \| germline clone (McCartney et al., 2006) cortical actin cytoskeleton (Zhou et al., 2011) cortical actin cytoskeleton & syncytial blastoderm embryo \| maternal effect (Webb et al., 2009) denticle belt \| maternal effect (McCartney et al., 2006) embryonic/first instar larval cuticle \| maternal effect (McCartney et al., 2006) embryonic/larval cuticle (Roberts et al., 2011, Roberts et al., 2012) embryonic/larval cuticle \| embryonic stage (Roberts et al., 2012, Zhou et al., 2011, Kunttas-Tatli et al., 2012) nucleus \| embryonic stage 4 \| germline clone (McCartney et al., 2006) organism \| embryonic stage 4 (Zhou et al., 2011) spindle & syncytial blastoderm embryo \| maternal effect (Webb et al., 2009)
Detailed Description
	Statement Reference Embryos that are both maternal and zygotic mutant for Apc2[g10] (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. (Kunttas-Tatli et al., 2012) 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. (Roberts et al., 2012) In maternal/zygotic Apc2[g10] 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 Apc2[g10] mutants expressing Apc2[ΔArmRepeats.T:Avic\GFP-EGFP] are lethal at the embryonic stage. Adult escapers are seen. 86% of Apc2[g10] mutants expressing Apc2[Armrepeatsonly.T:Avic\GFP-EGFP] are lethal at the embryonic stage. No adult escapers are seen. (Roberts et al., 2012) Homozygous embryos derived from homozygous females show 96% lethality at the embryonic stage. (Roberts et al., 2011) Embryos that are both maternal and zygotic mutant for Apc2[g10] (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. (Zhou et al., 2011) Embryos maternally mutant for Apc2[g10] 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. (Webb et al., 2009) There is no difference in the frequency of mispositioned oocytes between wild type and Apc2^g10 mutant germlines. 35% of Apc2^g10 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 Apc2^g10/+ mothers also show the nuclear retention phenotype. The cuticle of an average Apc2^g41 maternal/zygotic embryo shows an anterior hole, is 50-60% the length of wild-type and has at most 2 patches of denticles remaining. (McCartney et al., 2006) Asymmetric division of neuroblasts appears to be unaffected in the brains of Apc2^g10/Apc2^f90 larvae. Apc2^g10 has a more severe maternal effect embryonic phentype than either Apc2^ΔS or Apc2^d40. (Akong et al., 2002)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, suppressible \| partially by Apc2^{FL.T:Avic\GFP-EGFP} (Zhou et al., 2011, Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, suppressible \| partially by Apc2^{R1-R5SA.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, suppressible \| partially by Apc2^{R1-R5SD.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, suppressible \| partially by Apc2^{R3-R5ExR.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, suppressible \| partially by Apc2^{R3-R5SA.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, suppressible \| partially by Apc2^{R3-R5SD.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, suppressible \| partially by Apc2^{ΔC30.T:Avic\GFP-EGFP} (Zhou et al., 2011) Apc2^g10 has lethal \| embryonic stage phenotype, suppressible \| partially by Apc::Apc2^{APC2+APC1CT.T:Avic\GFP} (Roberts et al., 2012) Apc2^g10 has lethal \| embryonic stage phenotype, suppressible \| partially by Apc^{endsatSAMP.T:Avic\GFP} (Roberts et al., 2012) Apc2^g10 has lethal \| embryonic stage phenotype, suppressible \| partially by Apc^{WT.T:Avic\GFP} (Roberts et al., 2012)
NOT suppressed by
Statement Reference Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, non-suppressible \| partially by Apc2^{ΔC30.T:Avic\GFP-EGFP} (Zhou et al., 2011) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, non-suppressible by Apc2^{R1-R5ExR.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, non-suppressible by Apc2^{Δ15RΔ20RΔB.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype, non-suppressible by Apc2^{Δ20RΔB.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012)
Other
Statement Reference Apc2^g10, Apc^Q8 has cell shape defective \| somatic clone \| third instar larval stage phenotype (Roberts et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage \| germline clone \| rescuable maternal effect phenotype (Zhou et al., 2011, Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has lethal \| embryonic stage phenotype (Roberts et al., 2011, Roberts et al., 2012) Apc2^g10, Apc^Q8 has lethal \| larval stage phenotype (Akong et al., 2002, Akong et al., 2002, Akong et al., 2002, Akong et al., 2002) Apc2^g10, Apc^Q8 has neuroanatomy defective \| somatic clone \| third instar larval stage phenotype (Roberts et al., 2012)
Phenotype Manifest In
Enhanced by
Statement Reference Apc2^g10 has cortical actin cytoskeleton & syncytial blastoderm embryo \| maternal effect phenotype, enhanceable by dia[+]/dia^k07135 (Webb et al., 2009) Apc2^g10 has embryonic/larval cuticle \| embryonic stage phenotype, enhanceable by Apc^Q8 (Roberts et al., 2012)
NOT Enhanced by
Statement Reference Apc2^g10 has cortical actin cytoskeleton & syncytial blastoderm embryo \| maternal effect phenotype, non-enhanceable by Eb1^B13/Eb1[+] (Webb et al., 2009) Apc2^g10 has nucleus \| germline clone \| embryonic stage 4 phenotype, non-enhanceable by Apc^Q8 (McCartney et al., 2006)
Suppressed by
Statement Reference Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| embryonic stage phenotype, suppressible \| partially by Apc2^{ΔArmRepeats.T:Avic\GFP-EGFP} (Roberts et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| embryonic stage phenotype, suppressible by Apc2^{WT.T:Avic\GFP-EGFP} (Roberts et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, suppressible \| partially by Apc2^{FL.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, suppressible \| partially by Apc2^{R1-R5SA.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, suppressible \| partially by Apc2^{R1-R5SD.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, suppressible \| partially by Apc2^{R3-R5ExR.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, suppressible \| partially by Apc2^{R3-R5SA.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, suppressible \| partially by Apc2^{R3-R5SD.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, suppressible by Apc2^{FL.T:Avic\GFP-EGFP} (Zhou et al., 2011) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, suppressible by Apc2^{ΔC30.T:Avic\GFP-EGFP} (Zhou et al., 2011) Apc2^g10, Apc^Q8 has intestinal stem cell \| somatic clone phenotype, suppressible \| partially by pan^ΔN.Scer\UAS/Scer\GAL4^tub.PU (Lee et al., 2009) Apc2^g10 has embryonic/larval cuticle phenotype, suppressible \| partially by Apc::Apc2^{APC2+APC1CT.T:Avic\GFP} (Roberts et al., 2012) Apc2^g10 has embryonic/larval cuticle phenotype, suppressible \| partially by Apc^{endsatSAMP.T:Avic\GFP} (Roberts et al., 2012) Apc2^g10 has embryonic/larval cuticle phenotype, suppressible \| partially by Apc^{WT.T:Avic\GFP} (Roberts et al., 2012)
NOT suppressed by
Statement Reference Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, non-suppressible by Apc2^{R1-R5ExR.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, non-suppressible by Apc2^{Δ15RΔ20RΔB.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, non-suppressible by Apc2^{Δ20RΔB.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype, non-suppressible by Apc2^{ΔC30.T:Avic\GFP-EGFP} (Zhou et al., 2011) Apc2^g10 has cortical actin cytoskeleton & syncytial blastoderm embryo \| maternal effect phenotype, non-suppressible by Eb1^B13/Eb1[+] (Webb et al., 2009)
Enhancer of
Statement Reference Apc2^g10 is an enhancer of cortical actin cytoskeleton & syncytial blastoderm embryo \| maternal effect phenotype of dia^k07135 (Webb et al., 2009)
NOT Suppressor of
Statement Reference Apc2^g10/Apc2[+] is a non-suppressor of eye photoreceptor cell phenotype of Apc^Q8 (Takacs et al., 2008)
Other
Statement Reference Apc2^c9/Apc2^g10, Apc^Q8 has adult midgut \| heat sensitive phenotype (Lee et al., 2009) Apc2^g10, Apc^Q8, N^{dsRNA.P.Scer\UAS}, Scer\GAL4^tub.PU has intestinal stem cell \| somatic clone phenotype (Lee et al., 2009) Apc2^g10, Apc^Q8 has adult midgut \| somatic clone phenotype (Lee et al., 2009) Apc2^g10, Apc^Q8 has embryonic/larval cuticle \| germline clone \| rescuable maternal effect \| embryonic stage phenotype (Zhou et al., 2011, Kunttas-Tatli et al., 2012) Apc2^g10, Apc^Q8 has embryonic/larval cuticle phenotype (Roberts et al., 2011, Roberts et al., 2012) Apc2^g10, Apc^Q8 has medulla \| somatic clone \| third instar larval stage phenotype (Roberts et al., 2012) Apc2^g10, Apc^Q8 has spindle \| embryonic stage 4 phenotype (McCartney et al., 2006) Apc2^g10, Apc^Q8 has wing disc \| somatic clone \| third instar larval stage phenotype (Roberts et al., 2012)
Additional Comments
Genetic Interactions
Statement Reference 23% of embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[g10] and Apc[Q8]. All of the maternally and zygotically double mutant embryos die showing severe cuticle defects. Expression of Apc2[FL.T:Avic\GFP-EGFP] partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[Δ20RΔB.T:Avic\GFP-EGFP] fails to suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[Δ15RΔ20RΔB.T:Avic\GFP-EGFP] fails to suppress the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[R3-R5SA.T:Avic\GFP-EGFP] partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 68% of embryos are able to hatch. Expression of Apc2[R3-R5SD.T:Avic\GFP-EGFP] partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] germline clones and heterozygous double mutant males (generated using the FRT-FLP-DFS technique). 40% of embryos are able to hatch. Expression of Apc2[R1-R5SA.T:Avic\GFP-EGFP] partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[R1-R5SD.T:Avic\GFP-EGFP] partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[R1-R5ExR.T:Avic\GFP-EGFP] fails to suppress the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[R3-R5ExR.T:Avic\GFP-EGFP] partially suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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. (Kunttas-Tatli et al., 2012) The cells around the wing pouch in Apc2[g10] Apc[Q8] double mutant third instar larval wing disc clones are apically constricted and invaginated. Apc2[g10] Apc[Q8] 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. Apc[Q8] enhances the embryonic cuticle phenotype seen in Apc2[g10] mutants. In Apc2[g10] Apc[Q8] 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 Apc2[ΔArmRepeats.T:Avic\GFP-EGFP] provides a very weak rescue of the anterior fate loss seen in Apc2[g10] Apc[Q8] maternal/zygotic mutant embryos. Expression of Apc2[T:Avic\GFP-EGFP] rescues the anterior fate loss seen in Apc2[g10] Apc[Q8] maternal/zygotic mutant embryos. (Roberts et al., 2012) Embryos derived from Apc2[g10] Apc[Q8] 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 Apc2[g10] Apc[Q8] males crossed to females containing double homozygous germline clones are rescued by expression of Apc2[T:Avic\GFP-EGFP,T:Zzzz\Mito-actA]. The embryonic lethality is partially rescued (19% lethality is seen). The cuticle defects of embryos derived from Apc2[g10] Apc[Q8] males crossed to females containing double homozygous germline clones are strongly rescued by expression of Apc2[T: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 Apc2[g10] Apc[Q8] males crossed to females containing double homozygous germline clones are strongly rescued by expression of Apc2[T:Myr-Src64B,T:Avic\GFP-EGFP]. The embryonic lethality is partially rescued (33% lethality is seen). The cuticle defects of embryos derived from Apc2[g10] Apc[Q8] males crossed to females containing double homozygous germline clones are partially rescued by expression of Apc2[T:Avic\GFP-EGFP,T:Hsap\CAAX]. The embryonic lethality is not rescued. Apc[WT.T:Avic\GFP], Apc[endsatSAMP.T:Avic\GFP] and Apc::Apc2[APC2+APC1CT.T:Avic\GFP] each strongly rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2[g10] embryos derived from Apc2[g10] females). The embryonic lethality is also partially rescued (31%, 28% and 21% lethality is seen respectively) and viable adults are recovered. (Roberts et al., 2012) Embryos derived from Apc2[g10] Apc[Q8] 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 Apc2[g10] Apc[Q8] males crossed to females containing double homozygous germline clones are rescued by expression of Apc2[WT.T:Avic\GFP-EGFP], Apc2[ΔR3.T:Avic\GFP-EGFP] or Apc2[Δ15.T:Avic\GFP-EGFP]. The cuticle defects and lethality of embryos derived from Apc2[g10] Apc[Q8] males crossed to females containing double homozygous germline clones are not rescued by Apc2[KeepR3.T:Avic\GFP-EGFP], Apc2[Δ20.T:Avic\GFP-EGFP], Apc2[ΔR2.T:Avic\GFP-EGFP], Apc2[ΔB.T:Avic\GFP-EGFP] or Apc2[d40.T:Avic\GFP-EGFP]. Apc2[Δ15Δ20.T:Avic\GFP-EGFP] does not rescue the cuticle defects of embryos derived from Apc2[g10] Apc[Q8] males crossed to females containing double homozygous germline clones. Apc2[Δ15Δ20.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. Apc2[ΔSAMP.T:Avic\GFP-EGFP] does not rescue the cuticle defects of embryos derived from Apc2[g10] Apc[Q8] males crossed to females containing double homozygous germline clones. Apc2[ΔSAMP.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. (Roberts et al., 2011) 23% of embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[FL.T:Avic\GFP-EGFP] suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[ΔC30.T:Avic\GFP-EGFP] suppresses the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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 Apc2[N-SAMP.T:Avic\GFP-EGFP] is unable to suppress the lethality seen in embryos derived from females carrying homozygous Apc2[g10] Apc[Q8] 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. (Zhou et al., 2011) Apc2[g10], Apc[Q8]/Apc2[c9] 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, Apc2[g10], Apc[Q8] 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 Apc2[g10], Apc[Q8] double mutant clones are associated with gross anatomical changes, including hyperplasia and multilayered cellular masses that distort the luminal surface of the midgut. Apc2[g10], Apc[Q8] double mutant clones in the adult midgut that are also expressing N[dsRNA.P.Scer\UAS] under the control of Scer\GAL4[tub] 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 Apc2[g10], Apc[Q8] double mutant clones in the adult midgut that are also expressing N[dsRNA.P.Scer\UAS] under the control of Scer\GAL4[tub] compared to clones expressing N[dsRNA.P.Scer\UAS] under the control of Scer\GAL4[tub] in an otherwise wild-type background. The hyperplasia seen in Apc2[g10] Apc[Q8] double mutant intestinal stem cell clones in the adult midgut is partially suppressed if they are also expressing pan[ΔN.Scer\UAS] under the control of Scer\GAL4[tub]. (Lee et al., 2009) Apical actin in the offspring of Eb1[B13]/+; Apc2[g10] 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 dia[k07135]/+ ; Apc2[g10] 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. (Webb et al., 2009) The photoreceptor cell apoptosis phenotype seen in Apc^Q8 homozygotes is not suppressed by Apc2^g10/+. (Takacs et al., 2008) There is no difference in the frequency of mispositioned oocytes between wild type and Apc2^g10, Apc^Q8 double mutant mutant germlines. Apc2^g10, Apc^Q8 maternal/zygotic double mutant embryos show no defects in epithelial structure and do not show a total disruption of the cuticle. Apc2^g10, Apc^Q8 maternally mutant syncytial embryos show similar levels (35 vs 37%) of cortical nuclei movement to the anterior to Apc2^g10 syncytial embryos. Apc2^g10, Apc^Q8 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. (McCartney et al., 2006) Apc2^g10 Apc^Q8 double zygotic mutants are embryonic viable and exhibit a wild-type cuticle pattern, but die as larvae. (Akong et al., 2002) Apc2^g10, Apc^Q8 double homozygotes die as second instar larvae. (Akong et al., 2002)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Fails to complement	Apc2^ΔS (Akong et al., 2002, Akong et al., 2002)
Rescued by	Apc2^g10 is rescued by Apc2^{FL.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is rescued by Apc2^{R3-R5SA.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is rescued by Apc2^{R3-R5SD.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is rescued by Apc2^{WT.T:Avic\GFP-EGFP} (Roberts et al., 2012, Roberts et al., 2011) Apc2^g10 is rescued by Apc2^{ΔR3.T:Avic\GFP-EGFP} (Roberts et al., 2011)
Partially rescued by	Apc2^g10 is partially rescued by Apc2^{Armrepeatsonly.T:Avic\GFP-EGFP} (Roberts et al., 2012) Apc2^g10 is partially rescued by Apc2^cMa (McCartney et al., 2006, Webb et al., 2009) Apc2^g10 is partially rescued by Apc2^{FL.T:Avic\GFP-EGFP} (Zhou et al., 2011) Apc2^g10 is partially rescued by Apc2^{KeepR3.T:Avic\GFP-EGFP} (Roberts et al., 2011) Apc2^g10 is partially rescued by Apc2^{N-SAMP.T:Avic\GFP-EGFP} (Zhou et al., 2011) Apc2^g10 is partially rescued by Apc2^{R1-R5ExR.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is partially rescued by Apc2^{R1-R5SA.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is partially rescued by Apc2^{R1-R5SD.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is partially rescued by Apc2^{R3-R5ExR.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is partially rescued by Apc2^{T:Avic\GFP-EGFP,T:Hsap\CAAX} (Roberts et al., 2012) Apc2^g10 is partially rescued by Apc2^{T:Avic\GFP-EGFP,T:Mmmm\c-Ha-Ras} (Roberts et al., 2012) Apc2^g10 is partially rescued by Apc2^{T:Avic\GFP-EGFP,T:Zzzz\Mito-actA} (Roberts et al., 2012) Apc2^g10 is partially rescued by Apc2^{T:Myr-Src64B,T:Avic\GFP-EGFP} (Roberts et al., 2012) Apc2^g10 is partially rescued by Apc2^{Δ15.T:Avic\GFP-EGFP} (Roberts et al., 2011) Apc2^g10 is partially rescued by Apc2^{Δ15RΔ20RΔB.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is partially rescued by Apc2^{Δ20.T:Avic\GFP-EGFP} (Roberts et al., 2011) Apc2^g10 is partially rescued by Apc2^{Δ20RΔB.T:Avic\GFP-EGFP} (Kunttas-Tatli et al., 2012) Apc2^g10 is partially rescued by Apc2^{ΔArmRepeats.T:Avic\GFP-EGFP} (Roberts et al., 2012) Apc2^g10 is partially rescued by Apc2^{ΔB.T:Avic\GFP-EGFP} (Roberts et al., 2011) Apc2^g10 is partially rescued by Apc2^{ΔC30.T:Avic\GFP-EGFP} (Zhou et al., 2011) Apc2^g10 is partially rescued by Apc2^{ΔR1R4-R5.T:Avic\GFP-EGFP} (Roberts et al., 2011) Apc2^g10 is partially rescued by Apc2^{ΔR2.T:Avic\GFP-EGFP} (Roberts et al., 2011) Apc2^g10 is partially rescued by Apc2^{ΔR3-R5.T:Avic\GFP-EGFP} (Roberts et al., 2011)
Not rescued by	Apc2^g10 is not rescued by Apc2^{Δ15Δ20.T:Avic\GFP-EGFP} (Roberts et al., 2011)
Comments	Expression of Apc2[FL.T:Avic\GFP-EGFP] completely rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 98% hatch rate. Very weak cuticle defects are seen in the few embryos that fail to hatch. Expression of Apc2[Δ20RΔB.T:Avic\GFP-EGFP] partially rescues the lethality and cuticle phenotypes seen in embryos that are both maternally and zygotically mutant for Apc2[g10]. The level of rescue is dependent on the expression levels of the transgenes, with higher expression significantly reducing the degree of rescue. Expression of Apc2[Δ15RΔ20RΔB.T:Avic\GFP-EGFP] partially rescues the lethality and cuticle phenotypes seen in embryos that are both maternally and zygotically mutant for Apc2[g10]. The level of rescue is dependent on the expression levels of the transgenes, with higher expression significantly reducing the degree of rescue. Expression of Apc2[R3-R5SA.T:Avic\GFP-EGFP] significantly rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 93% hatch rate. Weak cuticle defects are seen in the few embryos that fail to hatch. Expression of Apc2[R3-R5SD.T:Avic\GFP-EGFP] significantly rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 97% hatch rate. Weak cuticle defects are seen in the few embryos that fail to hatch. Expression of Apc2[R1-R5SA.T:Avic\GFP-EGFP] partially rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 72% hatch rate. Very weak cuticle defects are seen in the embryos that fail to hatch. Expression of Apc2[R1-R5SD.T:Avic\GFP-EGFP] partially rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 89% hatch rate. Very weak cuticle defects are seen in the embryos that fail to hatch. Expression of Apc2[R1-R5ExR.T:Avic\GFP-EGFP] modestly rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 34% hatch rate. Weak cuticle defects are seen in the embryos that fail to hatch. Expression of Apc2[R3-R5ExR.T:Avic\GFP-EGFP] partially rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 91% hatch rate. Weak cuticle defects are seen in the embryos that fail to hatch. (Kunttas-Tatli et al., 2012) Apc2[T:Avic\GFP-EGFP,T:Zzzz\Mito-actA] rescues the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2[g10] embryos derived from Apc2[g10] females). The embryonic lethality of these Apc2 mutants is largely rescued (14% embryonic lethality is seen), and viable adults are obtained. Apc2[T:Avic\GFP-EGFP,T:Mmmm\c-Ha-Ras] and Apc2[T:Myr-Src64B,T:Avic\GFP-EGFP] each rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2[g10] embryos derived from Apc2[g10] females). The embryonic lethality of these Apc2 mutants is partially rescued (34% and 23% embryonic lethality is seen respectively), and viable adults are obtained. Apc2[T:Avic\GFP-EGFP,T:Hsap\CAAX] partially rescues the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2[g10] embryos derived from Apc2[g10] females). The embryonic lethality of these Apc2 mutants is not rescued. (Roberts et al., 2012) Expression of Apc2[ΔArmRepeats.T:Avic\GFP-EGFP] partially rescues the loss of anterior fates seen in maternal/zygotic Apc2[g10] mutant embryos. Denticle belts are largely restored to the cuticle. Expression of Apc2[Armrepeatsonly.T:Avic\GFP-EGFP] partially rescues the loss of anterior fates seen in maternal/zygotic Apc2[g10] mutant embryos. Expression of Apc2[T:Avic\GFP-EGFP] rescues the loss of anterior fates seen in maternal/zygotic Apc2[g10] mutant embryos. (Roberts et al., 2012) Apc2[WT.T:Avic\GFP-EGFP] and Apc2[ΔR3.T:Avic\GFP-EGFP] each rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2[g10] embryos derived from Apc2[g10] females). The embryonic lethality of these Apc2 mutants is also rescued, to adult viability. Apc2[ΔR1R4-R5.T:Avic\GFP-EGFP], Apc2[ΔR3-R5.T:Avic\GFP-EGFP], Apc2[Δ15.T:Avic\GFP-EGFP], Apc2[ΔR2.T:Avic\GFP-EGFP] and Apc2[ΔB.T:Avic\GFP-EGFP] each rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2[g10] embryos derived from Apc2[g10] 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. Apc2[KeepR3.T:Avic\GFP-EGFP] and Apc2[Δ20.T:Avic\GFP-EGFP] each significantly rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2[g10] embryos derived from Apc2[g10] females). The embryonic lethality of these Apc2 mutants is not rescued. Apc2[d40.T:Avic\GFP-EGFP], Apc2[ΔSAMP.T:Avic\GFP-EGFP] and Apc2[EndatB.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 Apc2[g10] embryos derived from Apc2[g10] females). No adults are recovered. Apc2[Δ15Δ20.T:Avic\GFP-EGFP] fails to rescue the cuticle defects of embryos lacking both maternal and zygotic Apc2[+] function (homozygous Apc2[g10] embryos derived from Apc2[g10] females). The embryonic lethality of these Apc2 mutants is also not rescued. (Roberts et al., 2011) Expression of Apc2[FL.T:Avic\GFP-EGFP] completely rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 96% hatch rate and a viable, fertile stock. Expression of Apc2[N-SAMP.T:Avic\GFP-EGFP] partially rescues the lethality seen in embryos that are both maternally and zygotically mutant for Apc2[g10], resulting in a 68% hatch rate. Fewer embryonic cuticle defects are also seen. Expression of Apc2[ΔC30.T:Avic\GFP-EGFP] completely rescues the lethality seen in embryos that are maternally and zygotically mutant for Apc2[g10], resulting in a viable, fertile stock. Expression of Apc2[FL.T:Avic\GFP-EGFP] significantly rescues the pseudocleavage furrow extension defects seen in embryos that are both maternally and zygotically mutant for Apc2[g10] (generated using the FRT-FLP-DFS technique). 7% of cortical actin rings in the four cortical divisions before cellularisation are incomplete. Expression of Apc2[ΔC30.T:Avic\GFP-EGFP] partially rescues the pseudocleavage furrow extension defects seen in embryos that are both maternally and zygotically mutant for Apc2[g10] (generated using the FRT-FLP-DFS technique). 38% of cortical actin rings in the four cortical divisions before cellularisation are incomplete. Expression of Apc2[N-SAMP.T:Avic\GFP-EGFP] partially rescues the pseudocleavage furrow extension defects seen in embryos that are both maternally and zygotically mutant for Apc2[g10] (generated using the FRT-FLP-DFS technique). 41% of cortical actin rings in the four cortical divisions before cellularisation are incomplete. (Zhou et al., 2011) Expression of the Apc2^cMa transgene partially rescues the nuclear retention phenotype of Apc2^g10 syncytial embryos - the penetrance of the phenotype falls from 35% to only 14% in rescued embryos. (McCartney et al., 2006)
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	Apc2 alleles can be divided into three categories based on their embryonic cuticle phenotypes, from weak to moderate to strong: Apc2^e90 = Apc2^b5 = Apc2^N175K < Apc2^c9 = Apc2^ΔS = Apc2^d40 < Apc2^g41 = Apc2^f90 = Apc2^g10. (McCartney et al., 2006)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	APC2^g10 (Roberts et al., 2012, Akong et al., 2002, Akong et al., 2002, Zimmerman et al., 2007, McCartney et al., 2006, Zhou et al., 2011, Roberts et al., 2012, Kunttas-Tatli et al., 2012, Roberts et al., 2011) Apc2^g10 (Takacs et al., 2008, Takacs et al., 2008, Lee et al., 2009, Webb et al., 2009)
Name Synonym
Secondary FlyBase IDs

References ( 14 )
Research paper	Kunttas-Tatli et al., 2012, Genetics 190(3): 1059--1075 Destruction complex function in the wnt signaling pathway of Drosophila requires multiple interactions between adenomatous polyposis coli 2 and armadillo. [FBrf0217816] Roberts et al., 2012, Mol. Biol. Cell 23(11): 2041--2056 Regulation of Wnt signaling by the tumor suppressor adenomatous polyposis coli does not require the ability to enter the nucleus or a particular cytoplasmic localization. [FBrf0218500] Roberts et al., 2012, PLoS ONE 7(2): e31284 Defining Components of the ßcatenin Destruction Complex and Exploring Its Regulation and Mechanisms of Action during Development. [FBrf0217546] Roberts et al., 2011, Mol. Biol. Cell 22(11): 1845--1863 Deconstructing the sscatenin destruction complex: mechanistic roles for the tumor suppressor APC in regulating Wnt signaling. [FBrf0213765] Zhou et al., 2011, J. Cell Sci. 124(9): 1589--1600 Cortical localization of APC2 plays a role in actin organization but not in Wnt signaling in Drosophila. [FBrf0213457] Lee et al., 2009, Development 136(13): 2255--2264 Adenomatous polyposis coli regulates Drosophila intestinal stem cell proliferation. [FBrf0208211] Webb et al., 2009, Development 136(8): 1283--1293 A novel role for an APC2-Diaphanous complex in regulating actin organization in Drosophila. [FBrf0207596] Takacs et al., 2008, Science 319(5861): 333--336 Dual positive and negative regulation of wingless signaling by adenomatous polyposis coli. [FBrf0202792] McCartney et al., 2006, Development 133(12): 2407--2418 Testing hypotheses for the functions of APC family proteins using null and truncation alleles in Drosophila. [FBrf0192526] Akong et al., 2002, Dev. Biol. 250(1): 91--100 Drosophila APC2 and APC1 play overlapping roles in wingless signaling in the embryo and imaginal discs. [FBrf0151886] Akong et al., 2002, Dev. Biol. 250(1): 71--90 Drosophila APC2 and APC1 have overlapping roles in the larval brain despite their distinct intracellular localizations. [FBrf0151885]
Supplementary material	Takacs et al., 2008, Science 319(5861): Supporting online material. [FBrf0202572]
Abstract	Zimmerman et al., 2007, A. Dros. Res. Conf. 48: 427A Genetic mosaic analysis reveals effects of APC2 APC1 double mutations during Drosophila wing development. [FBrf0198345] Zimmerman et al., 2006, A. Dros. Res. Conf. 47: 225B Genetic mosaic analysis reveals effects of APC2 APC1 double mutant clones during Drosophila wing development. [FBrf0188977]

Allele Dmel\Apc2g10

Allele Dmel\Apc2^g10