FlyBase Allele Report: Dmel\Apc2[N175K]

General Information

Symbol

Dmel\Apc2^N175K

Species

D. melanogaster

Name

FlyBase ID

FBal0148480

Feature type

allele

Associated gene

Dmel\Apc2

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Hamada and Bienz, 2002)

Mutagen

ethyl methanesulfonate

(Hamada and Bienz, 2002)

Progenitor genotype

Cytology

Description

Amino acid replacement: N175K.

(Hamada and Bienz, 2002)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3R:24,164,698..24,164,698 [+]

Nucleotide change:

T24164698R

Amino acid change:

N175K | Apc2-PA; N155K | Apc2-PB; N175K | Apc2-PC

Reported amino acid change:

N175K

(Hamada and Bienz, 2002)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 )

Disease

Evidence

References

model of intestinal cancer

CEA with Apc^Q8, Ras85D^V12.UAS

(Martorell et al., 2014, Martorell et al., 2014)

CEA with Apc^Q8, Ras85D^V12.cUa.UAS

(Parisi et al., 2023)

model of familial adenomatous polyposis 1

CEA with Apc^Q8

(Mendoza-Topaz et al., 2011)

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

Detailed Description

Statement

Reference

12% of Apc2^N175K 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 cuticle of an average Apc2^N175K maternal/zygotic embryo shows an anterior hole, is 50-60% the length of wild-type and has 3 patches of denticles remaining.

(McCartney et al., 2006)

Homozygous flies have wing vein and bristle defects and slightly rough eyes. Mutant females lay very few eggs and only some of these eggs develop through late embryonic stages. These escaper embryos produce cuticles that are completely naked on the ventral side. Ovaries of homozygous females contain very few mature egg chambers and oocytes are often underdeveloped in large chambers. The nurse cells tend to be irregularly arranged within maturing egg chambers. In 17% of egg chambers, the oocyte is mispositioned to one side of the anterior-posterior axis, rather than occupying the most posterior position of the egg chamber as in wild type. Mutant egg chambers have fewer membrane stacks in the plasma membranes of the germ cells than wild type, or abnormal stacks, showing long stretches of thin straight membrane interfaces that are devoid of membrane interdigitations. Cell vertices and ring canals also contain fewer membrane stacks than normal or abnormal membrane stacks, tending to have a flimsy appearance. There are numerous gaps between nurse cell membranes, especially at three-cell joins, the most abnormal of which have gaping holes. The number of spot adherens junctions is reduced to 31% of wild type in the epithelial cells of stage 6/7 embryos derived from Apc2^N175K parents. These embryos have extensive gaps between the lateral plasma membranes and large gaping holes at three-cell joins.

(Hamada and Bienz, 2002)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Apc2^N175K, Apc^Q8 has abnormal neuroanatomy | adult stage phenotype, suppressible by kug^N103-2/kug[+]

(Vien et al., 2024)

NOT Enhancer of

Statement

Reference

Apc2^N175K, Apc2^N175K, Apc^Q8, Apc^Q8 is a non-enhancer of increased occurrence of cell division | adult stage | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^NP7397

(Hudry et al., 2016)

Scer\GAL4^NP7397, Sxl^KK116156, Apc2^N175K, Apc2^N175K, Apc^Q8, Apc^Q8 is a non-enhancer of increased occurrence of cell division | adult stage | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^NP7397

(Hudry et al., 2016)

Suppressor of

Statement

Reference

Apc2^N175K/Apc^Q8 is a suppressor of abnormal neuroanatomy | semidominant | adult stage phenotype of kug^ΔICD.3xGFP

(Vien et al., 2024)

Other

Statement

Reference

Apc2^N175K, Apc^Q8 has abnormal neuroanatomy | adult stage phenotype

(Vien et al., 2024)

Apc2^N175K, Apc^Q8 has abnormal neuroanatomy | somatic clone | pupal stage phenotype

(Wang et al., 2019)

Apc2^N175K, Apc^Q8 has abnormal cell shape | somatic clone | pupal stage phenotype

(Wang et al., 2019)

Phenotype Manifest In

Enhanced by

Statement

Reference

Apc2^N175K has oocyte phenotype, enhanceable by Apc^Q8

(Hamada and Bienz, 2002)

Suppressed by

Statement

Reference

Apc2^N175K, Apc^Q8 has adult antennal lobe glomerulus phenotype, suppressible by kug^N103-2/kug[+]

(Vien et al., 2024)

Apc2^N175K, Apc^Q8 has adult antennal olfactory receptor neuron phenotype, suppressible by kug^N103-2/kug[+]

(Vien et al., 2024)

Apc2^N175K, Apc^Q8 has embryonic/larval cuticle | germline clone | rescuable maternal effect | embryonic stage phenotype, suppressible by Axn^UAS.GFP/Scer\GAL4^arm.PS

(Mendoza-Topaz et al., 2011)

Apc2^N175K, Apc^Q8 has embryonic/first instar larval cuticle phenotype, suppressible by Axn^UAS.GFP/Scer\GAL4^arm.PS

(Cliffe et al., 2003)

NOT Enhancer of

Statement

Reference

Apc2^N175K, Apc2^N175K, Apc^Q8, Apc^Q8 is a non-enhancer of adult posterior midgut epithelium | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^NP7397

(Hudry et al., 2016)

Scer\GAL4^NP7397, Sxl^KK116156, Apc2^N175K, Apc2^N175K, Apc^Q8, Apc^Q8 is a non-enhancer of adult posterior midgut epithelium | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^NP7397

(Hudry et al., 2016)

Suppressor of

Statement

Reference

Apc2^N175K/Apc^Q8 is a suppressor of adult antennal lobe glomerulus phenotype of kug^ΔICD.3xGFP

(Vien et al., 2024)

Apc2^N175K/Apc^Q8 is a suppressor of adult antennal olfactory receptor neuron phenotype of kug^ΔICD.3xGFP

(Vien et al., 2024)

Other

Statement

Reference

Apc2^N175K, Apc^Q8 has adult antennal olfactory receptor neuron phenotype

(Vien et al., 2024)

Apc2^N175K, Apc^Q8 has adult antennal lobe glomerulus phenotype

(Vien et al., 2024)

Apc2^N175K, Apc^Q8 has larval dorsal multidendritic neuron ddaC | somatic clone | pupal stage phenotype

(Wang et al., 2019)

Apc2^N175K, Apc^Q8 has dendrite | somatic clone | pupal stage phenotype

(Wang et al., 2019)

Apc2^N175K, Apc^Q8 has embryonic/larval cuticle | germline clone | rescuable maternal effect | embryonic stage phenotype

(Mendoza-Topaz et al., 2011)

Apc2^N175K, Apc^Q8 has embryonic/first instar larval cuticle phenotype

(Cliffe et al., 2003)

Additional Comments

Genetic Interactions

Statement

Reference

Apc2^N175K, Apc^Q8 double homozygous mutant clones (induced using Scer\FLP1^SOP.scE1x6) have a failure to prune all ddaC dendrites by 16 h after puparium formation (APF), unlike controls.

(Wang et al., 2019)

Clonal Apc2^N175K, Apc^Q8 double homozygosity alone or clonal Apc2^N175K, Apc^Q8 double homozygosity in combination with clonal Sxl^KK116156 co-expression do not enhance the increased mitotic index in the adult posterior midgut induced by the clonal expression of Ras85D^V12.UAS under the control of Scer\GAL4^esg-NP7397.

(Hudry et al., 2016)

Embryos maternally and zygotically double mutant for Apc^Q8 and Apc2^N175K display a naked cuticle phenotype.

Expression of Axn^{Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^arm.PS restores normal-looking denticle belts in embryos maternally and zygotically mutant for Apc^Q8 and Apc2^N175K.

(Mendoza-Topaz et al., 2011)

Apc^Q8, Apc2^N175K double mutant embryos have a naked cuticle phenotype.

(Cliffe et al., 2003)

The penetrance of the oocyte mislocalisation phenotype see in Apc2^N175K mutant females is increased to 32% if they are also mutant for Apc^Q8.

(Hamada and Bienz, 2002)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Apc2^ΔS

(Hamada and Bienz, 2002)

Partially rescued by

Apc2^N175K is partially rescued by Apc2^UAS.GFP/Scer\GAL4^arm.PS

(Hamada and Bienz, 2002)

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

7210

w^*; P{neoFRT}82B P{πM}87E sr¹ e¹ Apc2^N175K/TM3, Sb¹ Ser¹

7211

w^*; P{neoFRT}82B sr¹ e¹ Apc2^N175K Apc^Q8/TM3, P{ActGFP}JMR2, Ser¹

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 and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

APC2^N175K

(Wang et al., 2019)

Apc2^N175K

(Vien et al., 2024, Parisi et al., 2023, Campbell et al., 2019, Rahman et al., 2017, Hudry et al., 2016, Martorell et al., 2014, Martorell et al., 2014, Mattie et al., 2010, Christensen et al., 2009.5.6, McCartney et al., 2006)

N175K

(Bienz and Hamada, 2004, Hamada and Bienz, 2002)

apc2^N175K

(Ashour et al., 2023, Yamashita et al., 2003)

e-apc^N175K

(Mendoza-Topaz et al., 2011)

Name Synonyms

Secondary FlyBase IDs

References (18)

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