FB2024_03 , released June 25, 2024
Allele: Dmel\Atpα2206
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General Information
Symbol
Dmel\Atpα2206
Species
D. melanogaster
Name
FlyBase ID
FBal0048020
Feature type
allele
Associated gene
Dmel\Atpα
Associated Insertion(s)
P{PZ}Atpα2206
Carried in Construct
Also Known As
2206
Key Links
Allele class

hypomorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

hypomorphic allele - genetic evidence

(Palladino et al., 2003, Schubiger et al., 1994)
Mutagen
P-element activity
(Feng et al., 1997, Pavlidis and Tanouye, 1995, Schubiger et al., 1994)
Progenitor genotype
Associated Insertion(s)
P{PZ}Atpα2206
Cytology
Description

Insertion of a P{PZ} element into the first intron, approximately 8kb downstream of the exon 1-intron 1 border.

(Feng et al., 1997)

P{PZ} insertion into the first intron.

(Schubiger et al., 1994)
Allele components
Component
Use(s)
Inserted element
P{PZ}
Encoded product / tool
lacZ
Tagged with
Tag:NLS(P)
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  nervous system disease
      CEA
      (Palladino et al., 2003)
      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 neuroanatomy

      (Trotta et al., 2004)

      abnormal neuroanatomy | adult stage | recessive

      (Palladino et al., 2003)

      abnormal neurophysiology

      (Trotta et al., 2004, Pavlidis and Tanouye, 1995)

      bang sensitive

      (Palladino et al., 2003, Sun et al., 2001, Hurd et al., 1996, Pavlidis and Tanouye, 1995, Schubiger et al., 1994)

      bang sensitive (with AtpαDTS1)

      (Palladino et al., 2003)

      bang sensitive | heat sensitive, with AtpαD369N.hs

      (Sun et al., 2001)

      chemical sensitive

      (Sun et al., 2001)

      chemical sensitive | heat sensitive, with AtpαD369N.hs

      (Sun et al., 2001)

      decreased rate of movement

      (Sun et al., 2001)

      decreased rate of movement | heat sensitive, with AtpαD369N.hs

      (Sun et al., 2001)

      lethal | recessive

      (Feng et al., 1997)

      lethal - all die before end of pupal stage (with AtpαDTS2)

      (Palladino et al., 2003)

      lethal - all die during embryonic stage (with AtpαDTS1R1)

      (Palladino et al., 2003)

      lethal - all die during embryonic stage (with AtpαDTS1R2)

      (Palladino et al., 2003)

      lethal - all die during embryonic stage (with AtpαDTS2R1)

      (Palladino et al., 2003)

      lethal - all die during embryonic stage (with AtpαDTS2R2)

      (Palladino et al., 2003)

      lethal - all die during embryonic stage (with AtpαDTS2R3)

      (Palladino et al., 2003)

      lethal - all die during embryonic stage (with AtpαH64)

      (Palladino et al., 2003)

      paralytic

      (Palladino et al., 2003, Hurd et al., 1996, Schubiger et al., 1994)

      paralytic | conditional

      (Trotta et al., 2004)

      paralytic | heat sensitive (with AtpαDTS1)

      (Palladino et al., 2003)

      partially lethal - majority live (with Atpα01453a)

      (Palladino et al., 2003)

      short lived

      (Palladino et al., 2003)

      some die during embryonic stage (with AtpαDTS1R1)

      (Palladino et al., 2003)

      some die during embryonic stage (with AtpαDTS1R2)

      (Palladino et al., 2003)

      some die during embryonic stage (with AtpαDTS2R1)

      (Palladino et al., 2003)

      some die during embryonic stage (with AtpαDTS2R2)

      (Palladino et al., 2003)

      some die during embryonic stage (with AtpαDTS2R3)

      (Palladino et al., 2003)

      some die during embryonic stage (with AtpαH64)

      (Palladino et al., 2003)

      some die during pupal stage (with AtpαDTS2)

      (Palladino et al., 2003)
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Homozygous Atpα2206 mutants exhibit complete paralysis for >5 seconds after mechanical stress (10s vortex), after which animals slowly right themselves. Once Atpα2206 mutants achieve a standing position they are markedly sluggish for 1 to 3 minutes, grooming infrequently.

      In Atpα2206 mutants, the neuromuscular junction displays a 40% increase in bouton number.

      Evoked synaptic transmission and synaptic current amplitude is not significantly different in Atpα2206 mutants compared to controls. mEJC frequency in Atpα2206 mutants is more than doubled compared to controls, indicating a marked increase in presynaptic vesicular release probability. The average mEJC amplitudes in Atpα2206 mutants is not significantly different from controls, indicating normal postsynaptic responses to individual quanta. The distribution of mEJC amplitudes is unaltered. Elevation of "["Ca[2+]"]" to 2.0mM causes mEJC frequency and amplitude to increase as in controls.

      Atpα2206 mutants show synaptic fatigue properties indistinguishable from wild-type.

      Atpα2206 mutants do not exhibit significant attenuation in transmission amplitude compared to wild-type. The frequency of synaptic failures increases from zero at basal stimulation frequencies (0.5Hz) to over 50% after 3.5mins of 25Hz high frequency stimulation. Atpα2206 NMJs exhibit a 25-fold increase in synaptic transmission failure frequency compared to very infrequent failure in wild-type.

      Atpα2206 neurotransmission shows slightly impaired recovery from high-frequency stimulation-induced fatigue but is not significantly different from controls.

      In 2.0mM Ca[2+] saline, electrotonically elicited peak amplitudes are more than twofold larger in Atpα2206 mutants than in controls.

      During high-frequency electrotonic stimulation, Atpα2206 EJC amplitudes appear the same as controls.

      Using physiological extracellular "["Ca[2+]"]" (2.0mM), mEJC frequency is increased in Atpα2206 mutants compared to controls.

      Atpα2206 mutants show significantly increased mEJC frequencies at all "["Ca[2+]"]", compared to wild-type controls.

      Atpα2206 mutants are insensitive to activity-dependent mEJC amplitude modulation.

      Pre-synaptic vesicle endocytosis/exocytosis cycling is normal in Atpα2206 mutants.

      (Trotta et al., 2004)

      Atpα2206 adults are short lived and the brains of their middle-aged adults exhibit neurodegeneration, given the appearance of sporadically localized vacuolar pathology throughout the brain, which are rarely seen in controls.

      (Palladino et al., 2003)

      Homozygous flies are hypersensitive to ouabain in a feeding assay. Atpα2206 homozygotes that are also expressing AtpαD369N.hs are more sensitive to ouabain in a feeding assay than Atpα2206 homozygotes which do not carry AtpαD369N.hs. Atpα2206 homozygotes are paralysed for approximately 8 seconds following vigorous mechanical stimulation. This paralytic period is not altered following heat treatment. Atpα2206 homozygotes that are also expressing AtpαD369N.hs take longer to recover following paralysis than Atpα2206 homozygotes which do not carry AtpαD369N.hs. Atpα2206 homozygotes are less active than wild-type flies in a reactive climbing assay. This defect is more severe if the flies are also expressing AtpαD369N.hs.

      (Sun et al., 2001)

      Demonstrates bang sensitivity. Vortexing for 10 seconds causes 5-10 sec paralysis proceeding through staggering to normal behaviour over the course of 1-2 mins.

      (Hurd et al., 1996)

      Bang-sensitive mutant. Stimulation of the giant fibre (GF) can fail to evoke DLM potentials following the delivery of an electrical buzz (50-400 msec) to the brain. This failure lasts approximately 30 seconds.

      (Pavlidis and Tanouye, 1995)

      When flies are repeatedly knocked to the bottom of the vial they respond by going into paralysis for several seconds after which they recover completely. Flies vortexed for 10 seconds are paralysed for 5-10 seconds. Greater sensitivity to ouabain compared to wild type and a reduction in Na+ pump activity.

      (Schubiger et al., 1994)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressed by
      Statement
      Reference

      Atpα2206 has paralytic | conditional phenotype, suppressible by sesB1/sesB[+]

      (Trotta et al., 2004)

      Atpα2206 has paralytic | conditional phenotype, suppressible by parats1

      (Trotta et al., 2004)
      Suppressor of
      Statement
      Reference

      Atpα2206/Atpalpha[+] is a suppressor | partially of paralytic | conditional phenotype of sesB1

      (Trotta et al., 2004)
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      sesB1/Atpα2206 mutants exhibit a weaker stress-sensitive paralysis than either homozygous mutant alone, taking 3.6 seconds to achieve a standing position after stress.

      Atpα2206/parats1 double mutants display no significant paralysis after heat shock (90s, 30[o]C) and vortexing (10s).

      (Trotta et al., 2004)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Fails to complement

      AtpαDTS1

      (Palladino et al., 2003)

      AtpαDTS2

      (Palladino et al., 2003)

      AtpαDTS2R1

      (Palladino et al., 2003)

      AtpαDTS2R2

      (Palladino et al., 2003)

      AtpαDTS2R3

      (Palladino et al., 2003)

      AtpαH64

      (Palladino et al., 2003)

      AtpαDTS1R1

      (Palladino et al., 2003)

      AtpαDTS1R2

      (Palladino et al., 2003)

      Atpα01453a

      (Palladino et al., 2003)
      Partially rescued by

      Atpα2206 is partially rescued by Atpαhs.PS

      (Sun et al., 2001)
      Not rescued by

      Atpα2206 is not rescued by AtpαD369N.hs

      (Sun et al., 2001)
      Comments

      Atpαhs.PS partially rescues the ouabain sensitivity of Atpα2206 homozygotes. Atpα2206 homozygotes that are also expressing Atpαhs.PS recover more quickly following paralysis (induced by vigorous mechanical stimulation) than Atpα2206 homozygotes which do not carry Atpαhs.PS. The activity defects in a reactive climbing assay that are seen in Atpα2206 homozygotes are rescued if they are also expressing Atpαhs.PS.

      (Sun et al., 2001)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      Comments
      Comments

      Mobilisation of the P{PZ} insertion demonstrates it to be the cause of the bang sensitive phenotype and greater sensitivity to ouabain.

      (Schubiger et al., 1994)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (4)
      Reported As
      Symbol Synonym
      2206
      (Sun et al., 2001, Feng et al., 1997)
      ATPα 22006
      (Gautam et al., 2015)
      Atp a2206
      (Trotta et al., 2003)
      Atpα2206
      (Trotta et al., 2004)
      Name Synonyms
      Secondary FlyBase IDs
        References (11)