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General Information
Symbol
Dmel\Appld
Species
D. melanogaster
Name
FlyBase ID
FBal0028990
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

Interstitial deletion of the central region of the Appl gene.

Generated by translocation of distal part of Dp(1;Y)y+m64 onto proximal part of Df(1)yT7-518. Deletion of central portion of Appl gene. Exon containing translational start site and exon containing stop codon retained.

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
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Most Appld adults exhibit giant fibers with pruning defects, although it is not associated with synaptic transmission defects (10 trains of 10 stimulations at 100 Hz).

Appld mutants carrying Scer\GAL4Mef2.247.Switch exhibit an impairment in electric shock avoidance, as well as an apparent defect in learning that could result from the impairment in shock relativity.

Appld/+; Scer\GAL4Mef2.247.Switch/+ heterozygous flies exhibit a LTM impairment and a slight but significant STM defect compared with wild-type.

Appld/+; Scer\GAL4Mef2.247.Switch/+ heterozygous flies exhibit wild-type shock reactivity, wild-type olfactory acuity and normal learning.

Appld/+ flies have significant defects in short term memory (2hr) compared to controls in an olfactory aversive conditioning paradigm, but show normal learning, olfactory acuity and shock reactivity.

Adult specific expression of ApplAβ.Scer\UAS.T:Ivir\HA1 driven by Scer\GAL4Mef2.247.Switch (activated in adult flies fed RU486) significantly enhances short term memory defects in Appld/+ flies (compared to Appld/+ flies or to controls not fed RU486); there are no significant effects on learning, olfactory acuity or shock reactivity.

No vacuole formation is seen in the brains of Appld mutant flies up to 14 days old. However, some vacuoles are detected in the brains of 4 week old flies. This phenotype occurs with full penetrance and vacuoles are not seen in age matched controls. The lifespan of Appld mutant flies is significantly shortened; females live up to a maximum of 54 days compared to 54 days in controls and males only live to a maximum of 40 days compared to 102 days in controls. 7% of male and female flies have died by 8 days, compared to only 1% and 2% of females and males respectively.

Homozygous and Appld/Df(1)vndD38 adults have a normal central brain volume at 0 days after eclosion.

Mutants show loss of the scutellar macrochaetae.

EJC amplitude in Appld larvae is reduced compared to wild-type.

Appld larvae show enhanced post-tetantic potentiation.

Appld heterozygotes exhibit a reduction in bouton number.

Appld mutants exhibit a significant decrease in EJP amplitude compared to wild-type.

Appld flies do not show significantly impaired survival under standard conditions. However, these flies show a large increase in mortality compared to wild-type flies 1 and 2 weeks after brain trauma.

Mutant animals show a reduction in the number of scutellar and sternopleural mechanosensory organs.

Homozygous mutant larvae exhibit organelle accumulation within neurons. However the larvae are viable and do not exhibit tail flipping or paralysis.

NMJs from mutant larvae have a generally normal appearance but have 34% fewer boutons than wild type at muscles 6 and 7 of abdominal segment 3. Total number of synaptic boutons (muscles 6 and 7 (abdominal segment 3)) is decreased, percentage of satellite boutons is decreased and the number of normal boutons is decreased. When Applsd.Scer\UAS expression is driven in the motoneurons muscles 6 and 7 (abdominal segment 3) in combination with Appld total number of synaptic boutons is increased, percentage of satellite boutons is increased and the number of normal boutons is increased.

No morphological defects either externally or in parafin sections of heads. Abnormal fast phototactic response, not due to simple locomotor defect.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Appld/Appl[+] is a non-enhancer of neuroanatomy defective | dominant | adult stage phenotype of tapGal4

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Phenotype Manifest In
Suppressed by
NOT suppressed by
Statement
Reference

Appld has anterior scutellar bristle phenotype, non-suppressible by APP-BP1[+]/APP-BP1Ex183

Appld has posterior scutellar bristle phenotype, non-suppressible by APP-BP1[+]/APP-BP1Ex183

Appld has posterior scutellar bristle phenotype, non-suppressible by APP-BP1[+]/APP-BP1Ex62

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Appld/Appl[+] is a non-enhancer of adult mushroom body alpha-lobe | adult stage phenotype of tapGal4

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

Appld is a non-suppressor of ventral adult lateral neuron & axon phenotype of Scer\GAL4P2.4.Pdf, hepCA.UAS

Appld is a non-suppressor of ventral adult lateral neuron & axon phenotype of Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4P2.4.Pdf

Other
Additional Comments
Genetic Interactions
Statement
Reference

Appld/+ does not significantly enhance frequency of mushroom body beta lobe axon overgrowth defects in tapGal4/+ brains.

Expression of kuzScer\UAS.cFa in a Appld/+; Scer\GAL4Mef2.247.Switch heterozygous background exacerbates the short term memory deficit found in this background. These flies exhibit this exacerbated defect regardless of whether the flies are fed with RU for 48 hours before conditioning. Appld/+; Scer\GAL4Mef2.247.Switch/kuzScer\UAS.cFa flies fed with RU and testing immediately after conditioning exhibit wild-type learning. The ability to avoid electric shocks as well as their olfactory acuity to each odour after electric shock exposure is unaffected.

Adult specific expression of BaceScer\UAS.cCSa driven by Scer\GAL4Mef2.247.Switch (activated in adult flies fed RU486) significantly enhances short term memory defects in an olfactory aversive conditioning paradigm compared to Appld/+ flies or to controls not fed RU486; there are no significant effects on learning, olfactory acuity or shock reactivity.

Adult specific expression of BaceScer\UAS.cCSa driven by Scer\GAL4c739 (using the TARGET system) significantly enhances short term memory defects in an olfactory aversive conditioning paradigm compared to Appld/+ flies or to genetic or temperature controls; there are no significant effects on learning, olfactory acuity or shock reactivity.

Hemizygosity for Appld enhances the vacuolisation seen in 4 day old SNF4Aγloe mutant males.

Expression of ApplScer\UAS.cCSa under the control of Scer\GAL4Appl.G1a partially suppresses the vacuolisation seen in 4 day old Appld SNF4Aγloe double mutant males, returning the phenotype to the level seen in SNF4Aγloe single mutants.

Expression of Appls.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Appl.G1a fails to suppress the vacuolisation seen in 4 day old Appld SNF4Aγloe double mutant males.

yataKE2.1/yataKE2.1 Appld/Df(1)vndD38 double mutant adults show a significant reduction in central brain volume at 0 days after eclosion.

The reduction in lifespan seen in yataKE2.1 homozygous adults is more severe if the flies are also carrying Appld/Df(1)vndD38.

The loss of anterior scutellar macrochaetae that is seen in Appld flies is partially suppressed by APP-BP1Ex62/+, but is not suppressed by APP-BP1Ex183/+. The loss of posterior scutellar macrochaetae that is seen in Appld flies is not suppressed by APP-BP1Ex62/+ or APP-BP1Ex183/+.

Overexpression of Fas2Scer\UAS.cAa in both presynaptic and postsynaptic cells (under the control of Scer\GAL4C164 and Scer\GAL4C57) in Appld mutants leads to a wild-type number of boutons, in contrast to the two-fold increase when Appl levels are normal.

The increase in bouton number in Fas2e76/+ heterozygotes is completely suppressed in Appld homozygous mutants. Indeed, the number of synaptic boutons is lower than in wild-type.

The increased EJP amplitude in Fas2e76/+ heterozygotes is completely suppressed in the absence of Appl in Appld, Fas2e76/+ mutants. The EJP is indistinguishable from Appld/+ mutants.

Expression of hepCA.Scer\UAS, under the control of Scer\GAL4P2.4.Pdf, in an Appld mutant background still induces the significant axonal extension seen when the transgene is expressed in a wild-type background.

The addition of Appld enhances the adult brain degeneration phenotype seen in SNF4Aγloe animals.

Xenogenetic Interactions
Statement
Reference

Expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, under the control of Scer\GAL4P2.4.Pdf, in a Appld background still induces the axonal arborization phenotype that occurs when the transgene is expressed in a wild-type background.

Complementation and Rescue Data
Partially rescued by

Appld is partially rescued by Applhs.PL

Comments

Expression of wild-type ApplScer\UAS.cTa in the mushroom bodies, under the RU-fed control of Scer\GAL4Mef2.247.Switch rescues the STM deficit found in Appld/+ ; Scer\GAL4Mef2.247.Switch flies.

Expression of Appls.Scer\UAS in a heterozygous Appld/+;Scer\GAL4Mef2.247.Switch background suppresses the short term memory defect seen in this background, even in flies that have not been fed RU.

RU-induced expression of Applsd.Scer\UAS under the control of Scer\GAL4Mef2.247.Switch fails to rescue the long term memory deficit caused by Appld/+ partial loss-of-function.

Expression of Applsd.Scer\UAS in RU-fed flies suppresses the short-term memory defect found in Appld/+; Scer\GAL4Mef2.247.Switch flies. In contrast, in the absence of RU-feeding, Appld/+; Scer\GAL4Mef2.247.Switch/Applsd.Scer\UAS flies exhibit scores that are indistinguishable from controls and significantly lower than that found in wild-type flies.

RU-induced expression of Applsd.Scer\UAS under the control of Scer\GAL4Mef2.247.Switch fails to rescue the long term memory deficit caused by Appld/+ partial loss-of-function.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (22)