|Feature type||allele||Associated gene||Dmel\Atpα|
|Also Known As||ATPalphaDTS1|
|Map ( GBrowse )|
|Allele class||heat sensitive gain of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
comment=Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
pr_change=E982K|Atpalpha-PB,E982K|Atpalpha-PC,E982K|Atpa lpha-PE,E982K|Atpalpha-PF,E982K|Atpalpha-PG,E982K|Atpalpha -PH,E1021K|Atpalpha-PA
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: E982K.
|Phenotype Manifest In|
Heterozygous mutants have a significantly lower respiration (metabolic) rate than controls.
AtpαDTS1/+ flies show a significant reduction in lifespan compared to controls. AtpαDTS1 flies become instantly paralyzed upon exposure to a 15 minute 38oC heat shock. When returned to 22oC, >60% never recover and survivors only begin to show movement after over an hour at the permissive temperature.
AtpαDTS1/+ flies are sluggish compared to wild-type. After exposure to 37-38oC, 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 37-38oC. Although AtpαDTS1/+ flies do not show paralysis in response to mechanical shock when maintained and tested at 20-22oC, bang-sensitive paralysis does occur when flies are tested at 20-22oC if they have been maintained at 28oC. This phenomenon can occur for several hours after placing in the permissive temperature and paralysis lasts around 5-30 seconds. At elevated temperatures (37oC) continuous spiking activity is observed in thoracic readings taken from the dorsal flight muscles of AtpαDTS1 flies, but not in those of wild-type flies. AtpαDTS1 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 AtpαDTS1/+ 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.
|NOT Enhanced by|
AtpαDTS1 has short lived | dominant phenotype, non-enhanceable by Scer\GAL4hs.2sev/ShEKO.Scer\UAS.T:Avic\GFP-GL
|Phenotype Manifest In|
There is no additional reduction in lifespan in eag1, Sh14; AtpαDTS1 triple mutants compared to eag1, Sh14 mutants. The following heterozygous mutants do not enhance the shortened lifespan of AtpαDTS1/+ mutants: eag1, Sh14, and sei1. The short lived phenotype of AtpαDTS1 heterozygotes is enhanced in parats1/+, paraST109/+ and parats115/+ flies. In contrast, heterozygosity for either paralk5 or Df(1)D34 does not shorten the AtpαDTS1 life span. In addition to a shorter lifespan, parats1/+; AtpαDTS1/+ double mutants show an increase in the severity of spongiform neuropathology of the brain at 16 days compared to brains from parats1/+ or AtpαDTS1/+ single mutants. These double mutants show no significant change in temperature sensitivity compared to the single mutants. Like AtpαDTS1 single mutants, parats1; AtpαDTS1 mutants need several minutes to recover from a 3 minute 38oC heat shock. There is no significant change in the lifespan of AtpαDTS1 mutants when they express ShEKO.Scer\UAS.T:Avic\GFP-GL under the control of either Scer\GAL4elav.PLu or Scer\GAL4hs.2sev.
|Complementation & Rescue Data|
|Fails to complement|
|Stocks ( 0 )|
|Notes on Origin|
Selected as: a dominant temperature-sensitive paralytic mutation.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 3 )|
|Secondary FlyBase IDs|
|References ( 4 )|