FB2025_01 , released February 20, 2025
Allele: Dmel\lush1
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General Information
Symbol
Dmel\lush1
Species
D. melanogaster
Name
lush
FlyBase ID
FBal0093852
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Excision of the P{etau-lacZ}ET249 insertion removing 3kb of DNA, including the entire lush open reading frame.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 ( 0 )
Disease
Evidence
References
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
Phenotype Manifest In
Detailed Description
Statement
Reference

In lush1 mutants, at1 sensilla/Or67d show severely delayed activation in response to the pheromone cVA, as compared to controls.

Spontaneous firing of Or67d-expressing neurons is highly reduced in lush1 mutants compared to wild type.

lush1 Or67d-expressing olfactory sensory neurons show severely decreased spontaneous activity compared to control neurons.

T1 neurons from lush1 mutants do not respond to 11-cis vaccenyl acetate.

Behavioural attraction of lush1 mutant flies to wild-type males is significantly reduced compared to control flies. When female flies are used as bait, male flies show an increased attraction compared to females, but there is no difference in this attraction between wild-type and lush1 mutants. Substitution of male flies for 1% 11-cis vaccenyl acetate does not affect wild-type attraction. However lush1 mutants are completely defective for attraction to 11-cis vaccenyl acetate.

T1 neurons in lush1 mutants exhibit a greater than 400-fold reduction in spontaneous activity. Instead of one spike per second, the spontaneous activity in T1 neurons from lush1 mutants is approximately 1 spike every 430 seconds. No difference in spontaneous activity is observed in the T2 neurons of wild-type and lush1 mutants, despite an equivalent loss of lush protein from these sensilla.

No difference in mating latency, inappropriate mating behaviour, or mating stages is found in lush1 mutants compared to wild-type.

T2B neurons are defective for inhibition by high concentrations of ethanol and butanol in lush1 mutants. In wild-type T2B sensilla, at least one and usually several olfactory neurons within the sensillum reduce firing rates upon stimulation by concentrated butanol or ethanol. lush1 mutant T2B neurons do not show this normal inhibitory response to these odorants and continue firing at prestimulus rates. Low concentrations of these odorants have no effect on the activity of these neurons.

Mutant flies respond normally to both high and low concentrations of ethanol and ethyl acetate (they are attracted to low concentrations and repulsed by high concentrations) in a T-maze assay. Mutant flies show an abnormal response to benzaldehyde (BA) in a T-maze assay; they do not show the wild-type attraction to low concentrations of BA, while they are repulsed by high concentrations, as in wild type. The amplitude of neural response in the mushroom bodies in response to BA is similar in mutant and wild-type flies, even at the concentration of BA at which the behavioural defect is seen. Mutant flies show similar mushroom body activity patterns upon repetitive delivery of the same odour, similar to wild-type flies. However, the concentration-dependency of spatial distribution patterns which is seen in wild-type mushroom bodies in response to BA is abolished in mutant flies. As in wild type, ethyl acetate (EA) evokes concentration dependent patterns of distributed neural activity. Patterns evoked by different odours, as shown by comparisons among citral, octanol, EA and BA show similar odour specificity as in wild type.

Homozygous flies show an apparent increased attraction to ethanol, propanol and butanol in an olfactory trap assay compared to control flies. This abnormal response is specific to high odorant concentrations; attraction of flies to low concentrations of ethanol is similar to wild-type. Third instar larvae show a normal response to high concentrations of ethanol. The olfactory behaviour response to butanone, acetone, ethyl acetate, isoamyl acetate, acetic acid, benzaldehyde, methanol, isopropanol, pentanol and yeast is not significantly different from wild-type. Homozygous flies are defective for the avoidance behavioural response to concentrated ethanol which is present in wild-type flies. The electrical responses of ethanol-sensitive neurons to ethanol appear normal.

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

lush1 is a non-suppressor of abnormal smell perception phenotype of Snmp1Z0429

Phenotype Manifest In
NOT suppressed by
Statement
Reference

lush1 has prothoracic neuron phenotype, non-suppressible by Aper\APO-3lush.PX

lush1 has mesothoracic neuron phenotype, non-suppressible by Aper\APO-3lush.PX

lush1 has pit sensillum T1 phenotype, non-suppressible by Aper\APO-3lush.PX

lush1 has pit sensillum T2 phenotype, non-suppressible by Aper\APO-3lush.PX

Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Double mutants defective for lush1 SnmpZ0429 exhibit high spontaneous activity, indicating that Snmp functions downstream of lush in cVA signaling.

lush1 Snmp1/lush1 Snmp2 double mutant Or67d-expressing olfactory sensory neurons show an increase in spontaneous activity compared to control neurons, as is seen in Snmp1/Snmp2 single mutant neurons.

Xenogenetic Interactions
Statement
Reference

The presence of Aper\APO-3+t.lush fails to rescue the absence of response to 11-cis vaccenyl acetate found in lush1 mutant T1 neurons.

Complementation and Rescue Data
Rescued by
Comments

lush+tGa, lushF121A.tGa, lushD118A.tGa and lushF121W.tGa each restore the sensitivity of Or67d-expressing neurons to cis-vaccenyl acetate (cVA) in lush1 mutants. The neuronal response across a 10,0000-fold range of cVA concentrations is similar in all four cases, with the only statistically significant difference being observed at the highest cVA concentration (100%), where flies rescued with lushF121W.tGa or with lushD118A.tGa show a slightly lower cVA sensitivity than those rescued with lush+tGa.

lush+tGa, lushF121A.tGa, lushF121W.tGa and lushD118A.tGa each restore the spontaneous firing of Or67d-expressing neurons in lush1 mutants. There is no statistically significant difference in firing activity across the four genotypes.

The presence of lush+tKa rescues lush1 mutant T1 neuron responsiveness to 11-cis vaccenyl acetate.

lush1 mutant flies transformed with a copy of lush+tKa respond to 11-cis vaccenyl acetate and male flies in behavioural attraction assays.

Normal spontaneous activity rates are restored to T1 neurons upon introduction of lush+tKa.

lush1 mutants expressing lush+tKa have inhibitory responses to concentrated alcohol restored.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (13)