Allele Dmel\Atpα^DTS1

General Information
Symbol	Dmel\Atpα^DTS1	Species	D. melanogaster
Name		FlyBase ID	FBal0188150
Feature type	allele	Associated gene	Dmel\Atpα
Also Known As	ATPalpha^DTS1

Map ( GBrowse )
Allele class	heat sensitive gain of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	heat sensitive gain of function allele (Palladino et al., 2003)
Mutagen	ethyl methanesulfonate (Palladino et al., 2003)
Mutations Mapped to the Genome

Type Location Additional Notes References point mutation 3R:16,799,588..16,799,588 reported_pr_change=E982K comment=Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change. evidence=experimental na_change=G16799588A pr_change=E982K\|Atpalpha-PB,E982K\|Atpalpha-PC,E982K\|Atpa lpha-PE,E982K\|Atpalpha-PF,E982K\|Atpalpha-PG,E982K\|Atpalpha -PH,E1021K\|Atpalpha-PA (Palladino et al., 2003)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Atpα protein expression levels are normal in heterozygotes. (Ashmore et al., 2009) Amino acid replacement: E982K. (Palladino et al., 2003)
Cytology
Phenotypic Data
Phenotypic Class
	bang sensitive (with Atpα²²⁰⁶) (Palladino et al., 2003) bang sensitive \| dominant \| heat sensitive (Palladino et al., 2003) lethal \| embryonic stage (with Atpα^DTS1R1) (Palladino et al., 2003) lethal \| embryonic stage (with Atpα^DTS1R2) (Palladino et al., 2003) lethal \| embryonic stage (with Atpα^DTS2R1) (Palladino et al., 2003) lethal \| embryonic stage (with Atpα^DTS2R2) (Palladino et al., 2003) lethal \| embryonic stage (with Atpα^DTS2R3) (Palladino et al., 2003) lethal \| embryonic stage (with Atpα^H64) (Palladino et al., 2003) lethal \| embryonic stage \| recessive (Palladino et al., 2003) locomotor behavior defective \| adult stage (Palladino et al., 2003) neuroanatomy defective \| adult stage \| dominant (Palladino et al., 2003) neurophysiology defective \| heat sensitive (Palladino et al., 2003) paralytic \| dominant \| heat sensitive (Palladino et al., 2003) paralytic \| heat sensitive (Fergestad et al., 2006) paralytic \| heat sensitive (with Atpα^01453a) (Palladino et al., 2003) paralytic \| heat sensitive (with Atpα²²⁰⁶) (Palladino et al., 2003) paralytic \| heat sensitive (with Atpα^DTS2) (Palladino et al., 2003) partially lethal - majority die (with Atpα^01453a) (Palladino et al., 2003) partially lethal - majority die (with Atpα^DTS2) (Palladino et al., 2003) short lived (Palladino et al., 2003) short lived \| dominant (Fergestad et al., 2006)
Phenotype Manifest In
	adult brain (Palladino et al., 2003) dorsal medial muscle (Palladino et al., 2003) thoracico-abdominal ganglion (Palladino et al., 2003)
Detailed Description
	Statement Reference Heterozygous mutants have a significantly lower respiration (metabolic) rate than controls. (Ashmore et al., 2009) Atpα^DTS1/+ flies show a significant reduction in lifespan compared to controls. Atpα^DTS1 flies become instantly paralyzed upon exposure to a 15 minute 38^oC heat shock. When returned to 22^oC, >60% never recover and survivors only begin to show movement after over an hour at the permissive temperature. (Fergestad et al., 2006) Atpα^DTS1/+ flies are sluggish compared to wild-type. After exposure to 37-38^oC, these mutants become paralyzed within 10-30 seconds with complete penetrance. If this restrictive temperature is maintained for 3 minutes, then flies regain the ability to stand after 1-2 minutes at the permissive temperature and can only walk after another few minutes. Wild-type flies never become paralyzed from exposure to 37-38^oC. Although Atpα^DTS1/+ flies do not show paralysis in response to mechanical shock when maintained and tested at 20-22^oC, bang-sensitive paralysis does occur when flies are tested at 20-22^oC if they have been maintained at 28^oC. This phenomenon can occur for several hours after placing in the permissive temperature and paralysis lasts around 5-30 seconds. At elevated temperatures (37^oC) continuous spiking activity is observed in thoracic readings taken from the dorsal flight muscles of Atpα^DTS1 flies, but not in those of wild-type flies. Atpα^DTS1 flies have significantly shorter lifespans than wild type and become quite sedentary as they age, with a premature loss of both walking and flight activity. In the brains of middle-aged Atpα^DTS1/+ flies, neurodegeneration is evident as the appearance of vacuolar structures throughout the central brain and optic regions. Such structures are rarely seen in wild-type flies. The phenotype is age dependent as young adults (day 2-3 after eclosion) show little neuropathology. This age-dependent neurodegeneration can also be seen in the thoracic ganglion. (Palladino et al., 2003)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference Atpα^DTS1 has short lived \| dominant phenotype, enhanceable by para[+]/para^ts1 (Fergestad et al., 2006) Atpα^DTS1 has short lived \| dominant phenotype, enhanceable by para^ST109/para[+] (Fergestad et al., 2006) Atpα^DTS1 has short lived \| dominant phenotype, enhanceable by para^ts115/para[+] (Fergestad et al., 2006)
NOT Enhanced by
Statement Reference Atpα^DTS1 has short lived \| dominant phenotype, non-enhanceable by Df(1)D34/+ (Fergestad et al., 2006) Atpα^DTS1 has short lived \| dominant phenotype, non-enhanceable by eag[+]/eag¹ (Fergestad et al., 2006) Atpα^DTS1 has short lived \| dominant phenotype, non-enhanceable by para^lk5/para[+] (Fergestad et al., 2006) Atpα^DTS1 has short lived \| dominant phenotype, non-enhanceable by Scer\GAL4^hs.2sev/Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} (Fergestad et al., 2006) Atpα^DTS1 has short lived \| dominant phenotype, non-enhanceable by sei¹/sei[+] (Fergestad et al., 2006) Atpα^DTS1 has short lived \| dominant phenotype, non-enhanceable by Sh¹⁴/Sh[+] (Fergestad et al., 2006) Atpα^DTS1 has short lived \| dominant phenotype, non-enhanceable by Sh^{EKO.Scer\UAS.T:Avic\GFP-GL}/Scer\GAL4^elav.PLu (Fergestad et al., 2006)
Phenotype Manifest In
Enhanced by
Statement Reference Atpα^DTS1 has adult brain phenotype, enhanceable by para[+]/para^ts1 (Fergestad et al., 2006)
Enhancer of
Statement Reference Atpα^DTS1/Atpalpha[+] is an enhancer of adult brain phenotype of para^ts1 (Fergestad et al., 2006)
Additional Comments
Genetic Interactions
Statement Reference There is no additional reduction in lifespan in eag¹, Sh¹⁴; Atpα^DTS1 triple mutants compared to eag¹, Sh¹⁴ mutants. The following heterozygous mutants do not enhance the shortened lifespan of Atpα^DTS1/+ mutants: eag¹, Sh¹⁴, and sei¹. The short lived phenotype of Atpα^DTS1 heterozygotes is enhanced in para^ts1/+, para^ST109/+ and para^ts115/+ flies. In contrast, heterozygosity for either para^lk5 or Df(1)D34 does not shorten the Atpα^DTS1 life span. In addition to a shorter lifespan, para^ts1/+; Atpα^DTS1/+ double mutants show an increase in the severity of spongiform neuropathology of the brain at 16 days compared to brains from para^ts1/+ or Atpα^DTS1/+ single mutants. These double mutants show no significant change in temperature sensitivity compared to the single mutants. Like Atpα^DTS1 single mutants, para^ts1; Atpα^DTS1 mutants need several minutes to recover from a 3 minute 38^oC heat shock. There is no significant change in the lifespan of Atpα^DTS1 mutants when they express Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} under the control of either Scer\GAL4^elav.PLu or Scer\GAL4^hs.2sev. (Fergestad et al., 2006)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Fails to complement	Atpα^01453a (Palladino et al., 2003) Atpα²²⁰⁶ (Palladino et al., 2003) Atpα^DTS1R1 (Palladino et al., 2003) Atpα^DTS1R2 (Palladino et al., 2003) Atpα^DTS2 (Palladino et al., 2003) Atpα^DTS2R1 (Palladino et al., 2003) Atpα^DTS2R2 (Palladino et al., 2003) Atpα^DTS2R3 (Palladino et al., 2003) Atpα^H64 (Palladino et al., 2003)
Comments
Stocks ( 0 )

Notes on Origin
Discoverer
	Selected as: a dominant temperature-sensitive paralytic mutation. (Palladino et al., 2003)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	ATPalpha^DTS1 (Liu et al., 2012, Ashmore et al., 2009) Atpα^DTS1 DTS1 (Palladino et al., 2003)
Name Synonym
Secondary FlyBase IDs

References ( 4 )
Research paper	Liu et al., 2012, Neurobiol. Disease 45(1): 362--368 Genetically encoded redox sensor identifies the role of ROS in degenerative and mitochondrial disease pathogenesis. [FBrf0216742] Ashmore et al., 2009, Hum. Genet. 126(3): 431--447 Novel mutations affecting the Na, K ATPase alpha model complex neurological diseases and implicate the sodium pump in increased longevity. [FBrf0209097] Fergestad et al., 2006, Genetics 172(2): 1031--1042 Neuropathology in Drosophila membrane excitability mutants. [FBrf0190718] Palladino et al., 2003, J. Neurosci. 23(4): 1276--1286 Neural dysfunction and neurodegeneration in Drosophila Na[+]/K[+] ATPase α subunit mutants. [FBrf0159062]

Allele Dmel\AtpαDTS1

Allele Dmel\Atpα^DTS1