FlyBase Allele Report: Dmel\Atx2[X1]

General Information

Symbol

Dmel\Atx2^X1

Species

D. melanogaster

Name

FlyBase ID

FBal0141942

Feature type

allele

Associated gene

Dmel\Atx2

Associated Insertion(s)

Carried in Construct

Also Known As

Datx2^X1

Key Links

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Satterfield et al., 2002)

Progenitor genotype

P{EP}Atx2^EP3145

(Satterfield et al., 2002)

Cytology

Description

Imprecise excision of the P{EP} element, resulting in a 1.4kb deletion that removes the first 22 codons of the Atx2 coding sequence and extends into the first intron.

(Satterfield et al., 2002)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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 spinocerebellar ataxia type 2

CEA

(Bakthavachalu et al., 2018)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

ameliorates autosomal dominant cerebellar ataxia

modeled by Hsap\ATXN3^{tr.Q78.UAS.Tag:HA}

(Lessing and Bonini, 2008)

ameliorates amyotrophic lateral sclerosis

modeled by Hsap\TARDBP^UAS.cEa

(Elden et al., 2010)

model of spinocerebellar ataxia type 2

is ameliorated by Atx2^ΔcIDR

(Bakthavachalu et al., 2018)

is ameliorated by Atx2^ΔmIDR

(Bakthavachalu et al., 2018)

is ameliorated by Atx2^+t10.4

(Bakthavachalu et al., 2018)

ameliorates autosomal recessive intellectual developmental disorder

modeled by Nab2^ex3

(Rounds et al., 2022)

modeled by Nab2^EP3716

(Rounds et al., 2022)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

adult antennal lobe projection neuron | somatic clone

(Bakthavachalu et al., 2018)

adult thorax & chaeta, with Atx2^UAS.cSa

(Satterfield et al., 2002)

border follicle cell | germline clone

(Satterfield et al., 2002)

eye, with Atx2^UAS.cSa

(Satterfield et al., 2002)

eye | somatic clone

(Satterfield et al., 2002)

eye disc | somatic clone

(Satterfield et al., 2002)

nurse cell | germline clone

(Satterfield et al., 2002)

ommatidium, with Atx2^UAS.cSa

(Satterfield et al., 2002)

oocyte | germline clone

(Satterfield et al., 2002)

Detailed Description

Statement

Reference

Atx2^X1 adult antennal lobe projection neuron clones are of comparable size to control clones, but display far less stringent targeting of dendrites, growing across glomeruli borders and innervating multiple glomeruli as opposed to just one.

Adult Atx2^X1/Atx2⁰⁶⁴⁹⁰ transheterozygotes also bearing either Atx2^ΔmIDR or Atx2^ΔcIDR, but not Atx2^+t10.4, exhibit significantly lower long-term olfactory habituation, as compared to controls.

(Bakthavachalu et al., 2018)

Atx2^X1 mutant sensory neuron clones in the anterior wing margin (generated using MARCM) are retained at a similar rate to wild type at 6 days (83% in wild type and 75% in homozygous mutants).

(Lessing and Bonini, 2008)

Adult Atx2^X1 heterozygotes do not show any (age-related or otherwise) impairment in their climbing abilities compared to controls.

(Al-Ramahi et al., 2007)

Hemizygotes show second instar larval lethality. Homozygous clones in the retina result in severe loss of eye tissue. Eye discs of third instar larvae carrying homozygous retina clones are smaller than normal and have a disorganised ommatidial structure. Increased apoptosis is seen in these eye discs. Females carrying homozygous germ line clones are completely sterile and fail to lay eggs. Egg chambers in these females arrest prior to the cytoplasmic transport stage. The oocyte is often found in the middle of the egg chamber, or the oocyte is not specified at all. Columnar follicle cells are present in the vicinity of misplaced oocytes and the border cells migrate towards the misplaced oocytes. Atx2^X1 flies rescued by Atx2^Scer\UAS.cSa (in the absence of a Scer\GAL4 driver) are uncoordinated, can have a rough eye phenotype and have bent and forked thoracic sensory bristles. Many of the bristles have highly disorganised cuticular ridges and the actin bundles are shorter and thinner than normal. Homozygous clones result in bristles with shorter and thinner actin bundles than normal.

(Satterfield et al., 2002)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Atx2^X1/Atx2[+], Fmr1³ has abnormal learning | dominant phenotype, suppressible by Atx2^+t10.4

(Sudhakaran et al., 2014)

Atx2^X1/Atx2[+], Fmr1³ has abnormal learning | dominant phenotype, suppressible by Fmr1^+t14

(Sudhakaran et al., 2014)

AGO1^k08121/AGO1[+], Atx2^X1 has abnormal learning | dominant phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

Atx2^X1, me31B[+]/me31B^Δ2 has abnormal learning | dominant phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

Suppressor of

Statement

Reference

Atx2^X1/Atx2[+] is a suppressor | partially of visible | adult stage phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a suppressor of abnormal eye color phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a suppressor | partially of increased mortality during development phenotype of Nab2^ex3

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a suppressor | partially of abnormal neuroanatomy | adult stage phenotype of Nab2^ex3

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a suppressor of decreased cell number | somatic clone phenotype of Hsap\ATXN3^{tr.Q78.UAS.Tag:HA}, Scer\GAL4^elav-C155

(Lessing and Bonini, 2008)

Atx2^X1/Atx2[+] is a suppressor of decreased cell number | conditional phenotype of Hsap\ATXN3^{tr.Q78.UAS.Tag:HA}, Scer\GAL4^ninaE.PD

(Lessing and Bonini, 2008)

Atx2^X1 is a suppressor | partially of abnormal locomotor behavior | adult stage | progressive phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^nrv2.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+] is a suppressor | partially of abnormal locomotor behavior | adult stage | progressive phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^nrv2.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+] is a suppressor | partially of short lived phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^nrv2.PU

(Al-Ramahi et al., 2007)

Atx2^X1 is a suppressor of visible | adult stage phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

NOT Suppressor of

Statement

Reference

Atx2^X1/Atx2[+] is a non-suppressor of abnormal locomotor behavior | adult stage | progressive phenotype of Hsap\HTT^NT.128Q.UAS, Scer\GAL4^nrv2.PU

(Al-Ramahi et al., 2007)

Other

Statement

Reference

Atx2^X1/Atx2[+], Nab2^ex3 has partially lethal - majority live phenotype

(Rounds et al., 2022)

Atx2^X1/Atx2[+], Fmr1³ has abnormal learning | dominant phenotype

(Sudhakaran et al., 2014)

AGO1^k08121/AGO1[+], Atx2^X1 has abnormal learning | dominant phenotype

(McCann et al., 2011)

Atx2^X1, me31B[+]/me31B^Δ2 has abnormal learning | dominant phenotype

(McCann et al., 2011)

Phenotype Manifest In

Suppressed by

Statement

Reference

AGO1^k08121/AGO1[+], Atx2^X1 has antennal lobe glomerulus V phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

Atx2^X1, me31B[+]/me31B^Δ2 has antennal lobe glomerulus DM5 phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

Atx2^X1, me31B[+]/me31B^Δ2 has antennal lobe glomerulus V phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

AGO1^k08121/AGO1[+], Atx2^X1 has antennal lobe glomerulus DM5 phenotype, suppressible by Atx2^+t10.4

(McCann et al., 2011)

Atx2^X1/Atx2[+], Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU has eye | adult stage phenotype, suppressible by Atx2^UAS.cSa, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+], Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU has ommatidium | adult stage phenotype, suppressible by Atx2^UAS.cSa, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+], Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU has interommatidial bristle | adult stage phenotype, suppressible by Atx2^UAS.cSa, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+], Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU has retina | adult stage phenotype, suppressible by Atx2^UAS.cSa, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+], Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU has eye photoreceptor cell | adult stage phenotype, suppressible by Atx2^UAS.cSa, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Suppressor of

Statement

Reference

Atx2^X1/Atx2[+] is a suppressor | partially of eye phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a suppressor | partially of adult mushroom body alpha-lobe phenotype of Nab2^ex3

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a suppressor | partially of axon | adult stage phenotype of Nab2^ex3

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a suppressor of anterior wing margin | somatic clone phenotype of Hsap\ATXN3^{tr.Q78.UAS.Tag:HA}, Scer\GAL4^elav-C155

(Lessing and Bonini, 2008)

Atx2^X1/Atx2[+] is a suppressor of sensory neuron | somatic clone phenotype of Hsap\ATXN3^{tr.Q78.UAS.Tag:HA}, Scer\GAL4^elav-C155

(Lessing and Bonini, 2008)

Atx2^X1/Atx2[+] is a suppressor of photoreceptor | conditional phenotype of Hsap\ATXN3^{tr.Q78.UAS.Tag:HA}, Scer\GAL4^ninaE.PD

(Lessing and Bonini, 2008)

Atx2^X1/Atx2[+] is a suppressor of macrochaeta | adult stage phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^sca-109-68

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+] is a suppressor of eye | adult stage phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+] is a suppressor of ommatidium | adult stage phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+] is a suppressor of interommatidial bristle | adult stage phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+] is a suppressor of retina | adult stage phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+] is a suppressor of eye photoreceptor cell | adult stage phenotype of Hsap\ATXN1^82Q.UAS, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

NOT Suppressor of

Statement

Reference

Atx2^X1/Atx2[+] is a non-suppressor of ommatidium phenotype of Nab2^EP3716, Scer\GAL4^GMR.PU

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a non-suppressor of adult mushroom body beta-lobe phenotype of Nab2^ex3

(Rounds et al., 2022)

Atx2^X1/Atx2[+] is a non-suppressor of retina | adult stage | progressive phenotype of Hsap\HTT^NT.128Q.UAS, Scer\GAL4^GMR.PU

(Al-Ramahi et al., 2007)

Atx2^X1/Atx2[+] is a non-suppressor of photoreceptor neuron | adult stage | progressive phenotype of Hsap\HTT^NT.128Q.UAS

(Al-Ramahi et al., 2007)

Other

Statement

Reference

AGO1^k08121/AGO1[+], Atx2^X1 has antennal lobe glomerulus V phenotype

(McCann et al., 2011)

AGO1^k08121/AGO1[+], Atx2^X1 has antennal lobe glomerulus DM5 phenotype

(McCann et al., 2011)

Atx2^X1, me31B[+]/me31B^Δ2 has antennal lobe glomerulus V phenotype

(McCann et al., 2011)

Atx2^X1, me31B[+]/me31B^Δ2 has antennal lobe glomerulus DM5 phenotype

(McCann et al., 2011)

Additional Comments

Genetic Interactions

Statement

Reference

Fmr1³, Atx2^X1 double heterozygotes exhibit a complete block of the long-term habituation (LTH) normally seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days. LTH appears normal in either heterozygote alone. This loss of EB-evoked LTH is restored by expression of either Atx2^+t10.4 or Fmr1^+t14. Short term habituation following one hour exposure to EB appears normal.

(Sudhakaran et al., 2014)

AGO1^k08121, Atx2^X1 double heterozygotes exhibit a complete block of the long-term habituation (LTH) seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days. LTH appears normal in either heterozygote alone. This loss of EB-evoked LTH is restored by expression of Atx2^+t10.4. Short term habituation following one hour exposure to EB appears normal. LTH-associated structural plasticity is also blocked: although the V and DM5 glomeruli of Atx2^X1/+ flies show the expected growth following 4d of CO[[2]] or EB exposure, respectively, both the EB-evoked increase in DM5 volume and the CO[[2]]-induced increase in V are abolished in AGO1^k08121/+; Atx2^X1/+ double heterozygotes. These defects in structural plasticity are restored by Atx2^+t10.4.

me31B^Δ2, Atx2^X1 double heterozygotes exhibit a complete block of the long-term habituation (LTH) seen when flies are exposed to either ethyl butyrate (EB) or CO[[2]]] for 4 days. LTH appears normal in either heterozygote alone. This loss of EB-evoked LTH is restored by expression of Atx2^+t10.4. Short term habituation following 1 hour exposure to EB appears normal. LTH-associated structural plasticity is also blocked: although the V and DM5 glomeruli of Atx2^X1/+ flies show the expected growth following 4d of CO[[2]] or EB exposure, respectively, both the EB-evoked increase in DM5 volume and the CO[[2]]-induced increase in V are abolished in me31B^Δ2/+; Atx2^X1/+ double heterozygotes. These defects in structural plasticity are restored by Atx2^+t10.4.

(McCann et al., 2011)

Xenogenetic Interactions

Statement

Reference

One copy of Atx2^X1 suppresses the eye degeneration seen when Hsap\ATXN3^{tr.Q78.Scer\UAS.T:Ivir\HA1} is expressed in differentiated photoreceptor neurons under the control of Scer\GAL4^ninaE.PD. On average 6.9 visible photoreceptors are seen per ommatidium in 12 day old flies, similar to the 7 seen in controls. This compares to 6.4 when Hsap\ATXN3^{tr.Q78.Scer\UAS.T:Ivir\HA1} is expressed alone.

Homozygous Atx2^X1 suppresses the neuron loss seen in anterior wing margin clones induced in flies expressing Hsap\ATXN3^{tr.Q78.Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^elav-C155 (generated using MARCM). 77% of neurons are retained at 3 days, compared to only 13% when Hsap\ATXN3^{tr.Q78.Scer\UAS.T:Ivir\HA1} is expressed alone. 40% are recovered at 6 days, in contrast to the complete loss of neurons in Hsap\ATXN3^{tr.Q78.Scer\UAS.T:Ivir\HA1} expressing flies.

(Lessing and Bonini, 2008)

The age-progressive locomotor impairment and shorter adult life span characteristic for flies expressing Hsap\ATXN1^82Q.Scer\UAS under the control of Scer\GAL4^nrv2.PU as well as the loss of macrochaeta observed in flies expressing Hsap\ATXN1^82Q.Scer\UAS under the Scer\GAL4^sca-109-68 driver are significantly improved by combination with a Atx2^X1 in a heterozygous state.

Neither the age-progressive retina degeneration nor the decline of climbing abilities characteristic for adult flies expressing Hsap\HTT^{NT.128Q.Scer\UAS} under the control of the Scer\GAL4^GMR.PU or the Scer\GAL4^nrv2.PU driver, respectively, can be suppressed by combination with Atx2^X1 in a heterozygous state.

(Al-Ramahi et al., 2007)

Complementation and Rescue Data

Fails to complement

Atx2⁰⁶⁴⁹⁰

(Satterfield et al., 2002)

Rescued by

Atx2^X1 is rescued by Atx2^ΔmIDR

(Bakthavachalu et al., 2018)

Atx2^X1 is rescued by Atx2^ΔcIDR

(Bakthavachalu et al., 2018)

Atx2^X1/Atx2⁰⁶⁴⁹⁰ is rescued by Atx2^+t10.4

(Bakthavachalu et al., 2018)