FlyBase Allele Report: Dmel\Ank2[f02001]

General Information

Symbol

Dmel\Ank2^f02001

Species

D. melanogaster

Name

FlyBase ID

FBal0181704

Feature type

allele

Associated gene

Dmel\Ank2

Associated Insertion(s)

PBac{WH}Ank2^f02001

Carried in Construct

Also Known As

ank2²⁰⁰¹

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Associated Insertion(s)

PBac{WH}Ank2^f02001

Cytology

Description

Allele components

Component

Use(s)

Inserted element

PBac{WH}

misexpression element

Regulatory region(s)

UAS

binary expression system - regulatory region

Also carries

FRT

recombinase target site

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

3L:7,661,218..7,661,218 [+]

(Bulat et al., 2014, Keller et al., 2011, Koch et al., 2008, Pielage et al., 2008, Gene Disruption Project members and Exelixis, 2005)

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

Phenotype Manifest In

Detailed Description

Statement

Reference

Ank2^f02001/Ank2^f02001 mutant 1st, 2nd and 3rd instar larval neuromuscular junctions exhibit abberant microtubule organization, with aggregates of central microtubules; and a significant increase in synaptic retraction frequency at later larval stages, but no defect in the presence of microtubules at terminal boutons, as compared to controls.

(Stephan et al., 2015)

Ank2^f02001 mutants exhibit a significant increase in synaptic retractions compared with controls.

(Bulat et al., 2014)

Sound-evoked compound action potentials in the antennal nerve are not significantly different from wild type in mutant flies. However, nonlinear mechanical amplification is significantly reduced compared to wild type.

(Senthilan et al., 2012)

Ank2^f02001 mutant third instar larvae show severe NMJ degeneration, leading to complete elimination of the presynaptic nerve terminal at many NMJs. Loss of Ank2 also causes axonal blockages and severe disruption of the axonal and synaptic microtubule skeleton.

Homozygous egr^Δ25 mutants show large defects in EPSP amplitude compared to wild-type. A large number of recording are seen that have average EPSPs below 25mV.

(Keller et al., 2011)

Neuromuscular junctions of mutant larvae have fewer but larger boutons than normal.

Neuromuscular junctions of Ank2^RM5-1/Ank2^f02001 larvae have fewer but larger boutons than normal. The synaptic span (the widest extension of synaptic branches along a muscle fibre) is reduced compared to wild type.

(Koch et al., 2008)

Homozygotes die at late larval/early pupal stages.

Homozygotes show severe synaptic retractions at more than 60% of all neuromuscular junctions (NMJs) on muscles 6/7.

Ank2^f02001/Df(3L)RM5-2 and Ank2^f02001/Ank2^f00518 animals die as third instar larvae/early pupae, and they show severe synaptic retractions at the NMJs.

The severity of the synaptic retraction phenotype that is seen at the NMJs of Ank2^f02001/Df(3L)RM5-2 animals increases progressively during larval development.

Ank2^f02001/Df(3L)RM5-2 third instar larvae show defects in synaptic transmission and motoneuron excitability at the NMJ. Defects in in synapse morphology are also seen at the NMJ, with enlarged presynaptic membrane compartments. The presynaptic microtubule cytoskeleton shows abnormal organisation. Ultrastructurally, NMJs show hallmarks of synapse degeneration, including accumulations of endosomal/vacuole-like membrane profiles. In addition, giant synaptic boutons are seen at the NMJ. The boutons are elongated laterally, and multiple active zones can be detected. In addition, large vesicles are present. Large accumulations of microtubules can also be seen, with vesicles being absent from these regions.

(Pielage et al., 2008)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Ank2^f02001 has abnormal neurophysiology phenotype, suppressible | partially by Scer\GAL4^elav-C155/wgn^RNAi.UAS

(Keller et al., 2011)

Ank2^f02001 has abnormal neuroanatomy phenotype, suppressible by Dcp-1^Prev1

(Keller et al., 2011)

Ank2^f02001 has abnormal neuroanatomy phenotype, suppressible | partially by Dcp-1[+]/Dcp-1^Prev1

(Keller et al., 2011)

Ank2^f02001 has abnormal neuroanatomy phenotype, suppressible | partially by Debcl^E26

(Keller et al., 2011)

Ank2^f02001 has abnormal neuroanatomy phenotype, suppressible | partially by Dark^CD4

(Keller et al., 2011)

Ank2^f02001 has abnormal neuroanatomy phenotype, suppressible | partially by egr^Δ25

(Keller et al., 2011)

Ank2^f02001 has abnormal neuroanatomy phenotype, suppressible | partially by egr^RNAi.UAS/Scer\GAL4^egr-GAL4

(Keller et al., 2011)

Ank2^f02001 has abnormal neuroanatomy phenotype, suppressible | partially by Scer\GAL4^elav-C155/wgn^RNAi.UAS

(Keller et al., 2011)

Ank2^f02001 has abnormal neurophysiology phenotype, suppressible | partially by egr^Δ25

(Keller et al., 2011)

NOT suppressed by

Statement

Reference

Ank2^f02001 has abnormal neuroanatomy phenotype, non-suppressible by dl¹

(Keller et al., 2011)

Phenotype Manifest In

Enhanced by

Statement

Reference

Ank2^f02001 has synapse phenotype, enhanceable by CkIIα^LL05896

(Bulat et al., 2014)

Ank2^f02001 has neuromuscular junction phenotype, enhanceable by CkIIα^LL05896

(Bulat et al., 2014)

Ank2^f02001 has synapse phenotype, enhanceable by Scer\GAL4^elav-C155/CkIIα^{K66M.UAS.N.Tag:HA}

(Bulat et al., 2014)

Ank2^f02001 has neuromuscular junction phenotype, enhanceable by Scer\GAL4^elav-C155/CkIIα^{K66M.UAS.N.Tag:HA}

(Bulat et al., 2014)

Suppressed by

Statement

Reference

Ank2^f02001 has synapse phenotype, suppressible by Scer\GAL4^elav-C155/CkIIα^UAS.N.Tag:HA

(Bulat et al., 2014)

Ank2^f02001 has neuromuscular junction phenotype, suppressible by Scer\GAL4^elav-C155/CkIIα^UAS.N.Tag:HA

(Bulat et al., 2014)

Ank2^f02001 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible | partially by egr^Δ25

(Keller et al., 2011)

Ank2^f02001 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible | partially by egr^RNAi.UAS/Scer\GAL4^egr-GAL4

(Keller et al., 2011)

Ank2^f02001 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible | partially by Scer\GAL4^elav-C155/wgn^RNAi.UAS

(Keller et al., 2011)

Ank2^f02001 has embryonic/larval neuromuscular junction phenotype, suppressible by Dcp-1^Prev1

(Keller et al., 2011)

Ank2^f02001 has embryonic/larval neuromuscular junction phenotype, suppressible | partially by Dcp-1[+]/Dcp-1^Prev1

(Keller et al., 2011)

Ank2^f02001 has embryonic/larval neuromuscular junction phenotype, suppressible | partially by Debcl^E26

(Keller et al., 2011)

Ank2^f02001 has embryonic/larval neuromuscular junction phenotype, suppressible | partially by Dark^CD4

(Keller et al., 2011)

NOT suppressed by

Statement

Reference

Ank2^f02001 has microtubule | third instar larval stage phenotype, non-suppressible by egr^Δ25

(Keller et al., 2011)

Ank2^f02001 has axon | third instar larval stage phenotype, non-suppressible by egr^Δ25

(Keller et al., 2011)

Ank2^f02001 has microtubule | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav-C155/wgn^RNAi.UAS

(Keller et al., 2011)

Ank2^f02001 has axon | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav-C155/wgn^RNAi.UAS

(Keller et al., 2011)

Ank2^f02001 has embryonic/larval neuromuscular junction phenotype, non-suppressible by dl¹

(Keller et al., 2011)

Enhancer of

Statement

Reference

Ank2^f02001 is an enhancer of synapse phenotype of CkIIα^LL05896

(Bulat et al., 2014)

Ank2^f02001 is an enhancer of neuromuscular junction phenotype of CkIIα^LL05896

(Bulat et al., 2014)

Additional Comments

Genetic Interactions

Statement

Reference

Presynaptic expression of CkIIα^{Scer\UAS.N.T:Ivir\HA1} in Ank2^f02001 homozygous mutants significantly alleviates the synaptic retraction phenotype.

Presynaptic expression of CkIIα^{K66M.Scer\UAS.N.T:Ivir\HA1} in Ank2^f02001 homozygous mutants enhances the synaptic retraction phenotype.

Removal of one copy of CkIIα^P1 in a Ank2^f02001 homozygous background significantly increases the frequency of synaptic retractions.

Removal of one copy of Ank2^f02001 in a CkIIα^P1 homozygous background significantly increases the frequency of synaptic retractions.

(Bulat et al., 2014)

egr^Δ25 partially suppresses the NMJ degeneration seen in Ank2^f02001 mutant third instar larvae. The axonal blockages and microtubule disruption are not suppressed.

egr^Δ25 partially suppresses the synaptic transmission defects seen in Ank2^f02001 mutants. A near complete rescue in the number of small EPSPs is seen, however average EPSP amplitude is not completely restored to wild type levels.

Expression of egr^{dsRNA.Scer\UAS} under the control of Scer\GAL4^egr-GAL4 partially suppresses the NMJ degeneration seen in Ank2^f02001 mutant third instar larvae.

Expression of wgn^{dsRNA.Scer\UAS} under the control of Scer\GAL4^elav-C155 partially suppresses the NMJ degeneration seen in Ank2^f02001 mutant third instar larvae. The axonal blockages and microtubule disruption are not suppressed.

Expression of wgn^{dsRNA.Scer\UAS} under the control of Scer\GAL4^elav-C155 partially suppresses the synaptic transmission defects seen in Ank2^f02001 mutants. A near complete rescue in the number of small EPSPs is seen, however average EPSP amplitude is not completely restored to wild type levels.

Homozygous Dcp-1^Prev1 suppresses the NMJ degeneration seen in Ank2^f02001 mutants. One copy of Dcp-1^Prev1 is also able to partially suppress the phenotype.

Homozygous dl¹ does not suppress the NMJ degeneration seen in Ank2^f02001 mutant larvae.

Homozygous debcl^E26 partially suppresses the NMJ degeneration seen in Ank2^f02001 mutants.

Homozygous Ark^CD4 partially suppresses the NMJ degeneration seen in Ank2^f02001 mutants.

(Keller et al., 2011)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Ank2^f00518

(Pielage et al., 2008)

Not rescued by

Df(3L)RM5-2/Ank2^f02001 is not rescued by Scer\GAL4^unspecified/Ank2^S.UAS.Venus

(Pielage et al., 2008)

Df(3L)RM5-2/Ank2^f02001 is not rescued by Ank2^L8.UAS.Venus/Scer\GAL4^unspecified

(Pielage et al., 2008)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

18502

w¹¹¹⁸; PBac{WH}Ank2^f02001 CG32373^f02001/TM6B, Tb¹

Notes on Origin

Discoverer

Comments

Precise excision of the insertion reverts the neuromuscular junction phenotype.

(Koch et al., 2008)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

Ank2^f02001

(Miller et al., 2020, Weiner et al., 2020, Jegla et al., 2016, Bulat et al., 2014, Senthilan et al., 2012)

SP2523^f02001

ank2-L²⁰⁰¹

(Stephan et al., 2015)

ank2²⁰⁰¹

(Orr et al., 2020, Stephan et al., 2015, Nechipurenko and Broihier, 2012, Keller et al., 2011)

ank2^P2

(Bulat et al., 2014)

ank²⁰⁰¹

(Pielage et al., 2008)

ankyrin2²⁰⁰¹

(Mushtaq et al., 2022)

Name Synonyms

Secondary FlyBase IDs

References (13)

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