FlyBase Allele Report: Dmel\Acf[1]

General Information

Symbol

Dmel\Acf¹

Species

D. melanogaster

Name

FlyBase ID

FBal0157504

Feature type

allele

Associated gene

Dmel\Acf

Associated Insertion(s)

Carried in Construct

Also Known As

acf1¹

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Fyodorov et al., 2004)

Progenitor genotype

Acf^EP1181

(Fyodorov et al., 2004)

Cytology

Description

Imprecise excision of the P{EP}Acf1^EP1181 transposon deletes part of the first Acf1 intron and the beginning of the second exon.

(Fyodorov et al., 2004)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

3R:31,794,683..31,795,181 [+]

Comment:

Estimated endpoints of a 499 bp deletion resulting from the imprecise excision of P{EP}AcfEP1181. The deletion starts in the first intron and extends into the second exon of Acf.

(Fyodorov et al., 2004)

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 ( 0 )

Disease

Evidence

References

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

abnormal cell size

(Börner et al., 2016)

abnormal developmental rate | recessive

(Fyodorov et al., 2004)

abnormal mitotic cell cycle | recessive

(Fyodorov et al., 2004)

female semi-fertile

(Börner et al., 2016)

fertile | recessive

(Fyodorov et al., 2004)

increased cell death

(Börner et al., 2016)

increased cell death (with Df(3R)BSC687)

(Börner et al., 2016)

increased occurrence of cell division | embryonic stage

(Fyodorov et al., 2004)

increased occurrence of cell division | larval stage

(Fyodorov et al., 2004)

non-suppressor of variegation | recessive, with P{hsp26-pt-T}39C-5

(Fyodorov et al., 2004)

partially lethal - majority die | recessive

(Fyodorov et al., 2004)

suppressor of variegation | recessive, with In(1)w^m4h

(Fyodorov et al., 2004)

suppressor of variegation | recessive, with P{2212H6.5+PBX0.6}2L

(Fyodorov et al., 2004)

suppressor of variegation | recessive, with P{SUPor-P}KV0123

(Fyodorov et al., 2004)

viable | recessive

(Fyodorov et al., 2004)

Phenotype Manifest In

egg chamber

(Börner et al., 2016)

egg chamber (with Df(3R)BSC687)

(Börner et al., 2016)

embryo

(Fyodorov et al., 2004)

germarium

(Börner et al., 2016)

larval neuroblast | larval stage

(Fyodorov et al., 2004)

nurse cell

(Börner et al., 2016)

polar follicle cell

(Börner et al., 2016)

S phase

(Fyodorov et al., 2004)

Detailed Description

Statement

Reference

Acf¹/Acf¹ mutant females display a significant reduction in egg laying. A subset of Acf¹/Acf¹ mutant ovarioles display degeneration of the most posterior egg chamber, as shown by increased apoptosis in both oocyte and nurse cells. Abnormal apoptosis is not observed in the germarium and in stages 3-6. A small proportion of egg chambers also display cyst packaging defects at all stages of maturation, including the presence of two oocytes at opposite poles of the egg chamber, or 3-4 oocytes at opposing positions with nurse cells of different size and ploidy, evidence of multiple cysts being encapsulated by follicle cells, germaria with additional stalk-like structures, and egg chamber with additional, incorrectly positioned polar cells.

Acf¹/Df(3R)BSC687 mutants display egg chamber apoptosis and packaging defects.

(Börner et al., 2016)

About 60% of the expected homozygous progeny survive from heterozygous parents. Those that do are fertile and phenotypically normal. About 75% of progeny from homozygotes fail to pupariate and die in the third instar larval stage. Survivors committed to pupariation 1 to 2 days later than their wild-type counterparts. However viable escapers are produced, and these do not display significant defects in ovodeposition, larva hatching or adult eclosion. Homozygous embryos exhibit a shortening of their S phase leading to a shorter cell cycle, larval neuroblasts also exhibit an accelerated S phase and an increased mitotic index.

(Fyodorov et al., 2004)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

Acf¹ is an enhancer of visible | somatic clone phenotype of Iswi²

(Arancio et al., 2010)

Acf¹ is an enhancer of visible phenotype of Iswi^{K159R.UAS.Tag:HA}, Scer\GAL4^ey.PH

(Burgio et al., 2008)

Phenotype Manifest In

Enhancer of

Statement

Reference

Acf¹ is an enhancer of eye | somatic clone phenotype of Iswi²

(Arancio et al., 2010)

Acf¹ is an enhancer of eye phenotype of Iswi^{K159R.UAS.Tag:HA}, Scer\GAL4^ey.PH

(Burgio et al., 2008)

Other

Statement

Reference

Acf¹, Iswi² has abdomen phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi[+]/Iswi² has abdominal tergite 4 phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi[+]/Iswi² has abdominal tergite 5 phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi[+]/Iswi¹ has abdomen phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi[+]/Iswi¹ has abdominal tergite 4 phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi[+]/Iswi¹ has abdominal tergite 5 phenotype

(Fyodorov et al., 2004)

Acf¹, Df(3L)Pc has abdominal tergite 3 phenotype

(Fyodorov et al., 2004)

Acf¹, Df(3L)Pc has abdominal tergite 4 phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi² has abdominal tergite 5 phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi² has abdominal tergite 4 phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi¹ has abdomen phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi¹ has abdominal tergite 4 phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi¹ has abdominal tergite 5 phenotype

(Fyodorov et al., 2004)

Acf¹, Nap1^KG03959 has abdomen phenotype

(Fyodorov et al., 2004)

Acf¹, Nap1^KG03959 has abdominal tergite 4 phenotype

(Fyodorov et al., 2004)

Acf¹, Nap1^KG03959 has abdominal tergite 5 phenotype

(Fyodorov et al., 2004)

Acf¹, Iswi[+]/Iswi² has abdomen phenotype

(Fyodorov et al., 2004)

Additional Comments

Genetic Interactions

Statement

Reference

Acf1¹ enhances the eye defects seen in flies in which the eyes are homozygous for Iswi² in an otherwise heterozygous background (generated using the EGUF technique).

(Arancio et al., 2010)

The severity of the mutant eye phenotype caused by expression of Iswi^{K159R.Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^ey.PH is enhanced by Acf1¹.

(Burgio et al., 2008)

When heterozygous Iswi¹ or Iswi² is combined with homozygous Acf1¹, animals exhibit a homeotic transformation in the abdomen of males. This phenotype is manifested as ectopic reduced pigmentation of the abdominal A5 tergites, consistent with an A4 to A5 transformation. The penetrance (in Acf1¹/Acf1¹, Iswi²/+ animals) is 26%. In addition mutant flies often display an aberrant, asymmetric segmentation of the lower abdomen. When homozygous Nap1^KG03959 is combined with homozygous Acf1¹, animals exhibit a homeotic transformation in the abdomen of males. This phenotype is manifested as ectopic reduced pigmentation of the abdominal A5 tergites, consistent with an A4 to A5 transformation. The penetrance of this phenotype is 62%. In addition mutant flies often display an aberrant, asymmetric segmentation of the lower abdomen. The combination of Df(3L)Pc heterozygotes and Acf1¹ leads to a stronger extra sex combs phenotype than seen in Df(3L)Pc alone. 61% (compared to 18% in controls) of males have extra sex combs on the second and/or third pairs of legs. In addition over half of males exhibit ectopic pigmentation of their A3 and A4 abdominal tergites.

(Fyodorov et al., 2004)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially rescued by

Acf¹ is partially rescued by Acf^{Tag:TY1,EGFP,Tag:FLAG}

(Börner et al., 2016)

Acf¹ is partially rescued by Acf^{N.Tag:TY1,EGFP,Tag:FLAG}

(Börner et al., 2016)

Not rescued by

Acf¹ is not rescued by Acf^{C.Tag:TY1,EGFP,Tag:FLAG}

(Börner et al., 2016)

Comments

Expression of Acf^{C.T:Scer\TY1,T:Avic\GFP-EGFP,T:Zzzz\FLAG} does not rescue the apoptotic egg chamber phenotypes of Acf¹/Acf¹ mutants.

Expression of Acf^{N.T:Scer\TY1,T:Avic\GFP-EGFP,T:Zzzz\FLAG} rescues the apoptotic egg chamber phenotypes, but not the egg chamber cell packaging defects of Acf¹/Acf¹ mutants.

The presence of Acf^{T:Scer\TY1,T:Avic\GFP-EGFP,T:Zzzz\FLAG}/Acf^{T:Scer\TY1,T:Avic\GFP-EGFP,T:Zzzz\FLAG} fully rescues the egg chamber apoptotic defects, and partially rescues the egg chamber cell packaging defects of Acf¹/Acf¹ mutants.

(Börner et al., 2016)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (6)

Reported As

Symbol Synonym

Acf1¹

(Börner et al., 2016, Debruhl et al., 2013)

Acf1[1]

(Chioda et al., 2010)

Acf¹

Df(3R)acf¹

(Fyodorov et al., 2004)

acf1¹

(Arancio et al., 2010, Burgio et al., 2008)

acf¹

(Fyodorov et al., 2004)

Name Synonyms

Secondary FlyBase IDs

References (8)

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