FB2025_01 , released February 20, 2025
Allele: Dmel\nompC3
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General Information
Symbol
Dmel\nompC3
Species
D. melanogaster
Name
FlyBase ID
FBal0008344
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
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Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Nucleotide substitution: A2860T.

Amino acid replacement: K747term.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

A5357976T

Reported nucleotide change:

A2860T

Amino acid change:

K747term | nompC-PD; K747term | nompC-PE; K747term | nompC-PF; K747term | nompC-PG; K747term | nompC-PH

Reported amino acid change:

K747term

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
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Marker for
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Reporter construct used in assay
Human Disease Associations
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Disease
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Disease
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Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

nompC3/nompCf00642 mutant adult females have no difference in preference for softer plain, or 100 mM sucrose-containing, agarose for egg laying, compared to controls.

nompC3 mutant adults have significantly reduced spiking and mechanotransduction currents of mechanosensory neurons of the labellar taste bristles and labellar taste pegs in response to mechanical stimuli, compared to controls; there is no effect on depolarization of bristle mechanosensory neurons in response to current injections, compared to controls.

nompC1/nompC3 mutant larvae show a significantly decreased response to gentle touch, as compared to controls.

nompC3/nompCf00642 starved adult males have significantly reduced preference for softer sucrose-containing agarose, compared to controls; these transheterozygotes do not have significant alterations in exploratory behavior or sucrose preference, compared to controls.

nompC3/nompCf00642 adults have significant reductions in activity (spiking) of the L2 and L3 labellar sensilla in response sucrose stimulation and significant reductions in activity (spiking) of the L3, but not L2, labellar sensilla in response to mechanical stimulation, compared to controls; nompC1/nompC3 adults have significant reductions in activity (spiking) of the L2 and L3 labellar sensilla in response mechanical stimulation and significant reductions in activity (spiking) of the L2, but not L3, labellar sensilla in response to sucrose stimulation, compared to controls; nompC1/nompC3 adults also have a severe lack of coordination and die soon after hatching.

nompC1/nompC3 class III da neurons do not respond electrophysiologically to mechanical stimulation, and third instar larvae have a reduced response to gentle touch.

nompC1/nompC3 mutant larvae have a significant increase in defecation interval compared to controls.

nompC1/nompC3 flies show severely uncoordinated movements and very low locomotion speed.

nompC1/nompC3 mutant larvae show defects in the behavioural response to gentle touch. These larvae also show less of an increase in action potential frequency and a reduced increase in internal calcium levels in response to the stimulus.

Cho neurons in nompC1/nompC3 mutants do not respond to a low level of sound that is sufficient to trigger a Ca[2+] response in Cho neurons of wild-type larvae; however, a higher level of sound stimulation elicits a response, although this is still weaker than in controls.

Most homozygotes die at the third instar stage.

nompC1/nompC3 larvae show a prolonged stride duration (the average time needed to complete a single peristaltic contraction cycle) with normal stride size when their locomotion is compared to wild-type controls.

Crawling speed of homozygous and nompC1/nompC3 larvae is reduced compared to controls.

nompC1/nompC3 adults show severe defects in walking behaviour.

nompC2/nompC3 third instar larvae show the same preference for 17.5[o]C over 14[o]C in a two-way choice test as do wild-type controls.

nompC3/nompC4 mutants retain a preference for 18[o]C (i.e. are thermotactic).

Flies show severe uncoordination. Mechanoreceptor currents are reduced to 10% of normal. Action potentials are almost completely abolished.

External Data
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Xenogenetic Interactions
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Complementation and Rescue Data
Comments

Expression of nompCL.Scer\UAS.T:Avic\GFP (but not nompCΔ29ANK.Scer\UAS.T:Avic\GFP, nompCΔ12ANK.Scer\UAS.T:Avic\GFP or nompC29+17ARs.Scer\UAS.T:Avic\GFP-EGFP) driven by Scer\GAL419-12 rescues the electrophysiological and locomotor deficits in response to touch of nompC1/nompC3 third instar larvae; expression of nompC29+29ARs.Scer\UAS.T:Avic\GFP-EGFP leads to partial rescue.

Expression of either nompCL.Scer\UAS or nompCE1511A.Scer\UAS under the control of Scer\GAL4nompC.PC rescues the reduced locomotion of nompC1/nompC3 adults.

Expression of nompCD1516A.Scer\UAS under the control of Scer\GAL4nompC.PC partially but significantly rescues the reduced locomotion of nompC1/nompC3 adults.

Expression of nompCL.Scer\UAS under the control of Scer\GAL419-12 rescues the touch sensitivity defects seen in nompC1/nompC3 mutant larvae. The defects in behavior, action potential frequency and calcium response are all rescued.

The lethality of nompC1/nompC3 larvae is rescued by expression of nompCL.Scer\UAS under the control of Scer\GAL4nompC.PC. The reduced crawling speed and increased stride duration seen in nompC1/nompC3 larvae is also rescued.

The reduced crawling speed and increased stride duration of nompC1/nompC3 larvae is rescued by expression of nompCL.Scer\UAS under the control of either Scer\GAL45-40, Scer\GAL421-7 or Scer\GAL42-21.

The walking defects seen in nompC1/nompC3 adults are rescued by expression of nompCL.Scer\UAS under the control of either Scer\GAL421-7 or Scer\GAL4nompC.PC.

The reduced crawling speed of nompC1/nompC3 larvae is rescued by expression of nompCL.Scer\UAS.T:Avic\GFP under the control of Scer\GAL42-21.

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Notes on Origin
Discoverer
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Comments

Due to a naming clash that goes back many years, two different alleles of nompC, with contrasting molecular lesions, were named nompC[3]. Thanks to user input, we have been able to disambiguate these two alleles. They are now called nompC[3] and nompC[b19]. The nompC[3] allele was generated in the Zuker lab by EMS (FBrf0127378). The nompC[b19] allele was made by Szidonya and Reuter (FBrf0047784) and published in 1988 as jf24[b19]. Allele jf24[b19] was renamed in Lindsley and Zimm 1992 (p. 353) as l(2)25Dc[3]. Allele l(2)25Dc[3] subsequently became nompC[3] based on a foot note in Kernan et al., 1994 (FBrf0073546) identifying l(2)25Dc as nompC. The references and data for jf24[b19]/l(2)25Dc[3]/nompC[3] have now been split from the nompC[3] FlyBase record and are associated with allele nompC[b19].

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (26)