FB2024_03 , released June 25, 2024
Allele: Dmel\Nrgl10
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General Information
Symbol
Dmel\Nrgl10
Species
D. melanogaster
Name
FlyBase ID
FBal0013175
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
nrg3, l(1)B4
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description
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
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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

axon & mechanosensory neuron & adult head | conditional ts

axon & ocellus sensory structure | conditional ts

Detailed Description
Statement
Reference

Nrgl10 single mutants exhibit mild defects in motoneuron intersegmental nerve axon guidance.

Nrgl10 single mutants do not display any aCC or RP2 exit phenotypes.

Homozygous females are viable at 18[o]C, but do not survive at 25 or 29[o]C.

Nrgl10/Nrgibx females are viable at 18 and 25[o]C.

Nrgl10/Nrgl4 and Nrgl10/Nrgl7 females are viable at 18[o]C but are inviable at 25[o]C.

NrgG0099/Nrgl10 flies are viable at 18[o]C and rare escapers are seen at 25[o]C.

NrgG0413/Nrgl10 and NrgG0488b/Nrgl10 females are inviable at both 18 and 25[o]C.

Nrgl10/Nrg849 and Nrgl10/Nrg892 females show normal sexual receptivity at 18 and 25[o]C, but show reduced receptivity at 29[o]C when mated to wild-type males.

Homozygous embryos raised at the restrictive temperature show altered motoneuron pathfinding trajectories.

When Nrgl10 embryos and larvae are raised at the permissive temperature (17oC) and shifted to the restrictive temperature (29oC) during early to middle third instar larvae, abnormalities are seen in ocellar sensory system (OSS) axon pathfinding without alterations in cell number or position. Ocellar pioneer (OP) axons become attached to the epidermis, where they can fasciculate with bristle mechanosensory (BM) axons. Secondly OP axons fail to cross the brain at the appropriate choice point. After head eversion, this alteration is revealed as an OP nerve projecting inside the head. free and away from the epidermis but heading and terminating at an ectopic position. Thirdly BM axons take abnormal trajectories. Although they initially project in the correct direction, sometimes when reaching the region where they should leave the epidermal surface and project to the brain, they turn backward and project away from their normal trajectory. Forth BM axons sometimes stall in the epidermis. Fifth, some BM axons, affter head eversion, project separated from the epidermis.

Homozygotes are viable at 18oC and 21oC. At 25oC, viability of homozygous embryos is 22% and those embryos that do hatch die as first instar larvae shortly after hatching. No homozygous embryos survive to hatching at 29oC. The temperature-sensitive period for lethality is between midstage 15 and late stage 16 of embryonic development. Homozygous embryos show a general disorganisation of the peripheral nervous system cell bodies when raised at the restrictive temperature of 29oC. The lateral pentascolopidial chordotonal organ (lch5) cells are rounded and irregularly positioned. The apical dendrites and basal anchoring process are disorganised. The disorganisation of the lch5 appears to displace most of the other cells of the lateral cluster, including the lateral campaniform sensilla, the lateral trichoid sensilla and the lateral monoscolopidial chordotonal organ. Fasciculation of the peripheral sensory axon tracts appears relatively normal. The aCC and SNb motoneurons often show a stalled phenotype, failing to extend normally, and SNb motoneurons sometimes show abnormal contacts with their targets.

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

Nrgl10 has axon & mechanosensory neuron & adult head | conditional ts phenotype, enhanceable by Scer\GAL4MS1075/htlλ.UAS

Nrgl10 has axon & ocellus sensory structure | conditional ts phenotype, enhanceable by Egfrunspecified

Nrgl10 has axon & mechanosensory neuron & adult head | conditional ts phenotype, enhanceable by Egfrunspecified

Suppressed by
Statement
Reference

Nrgl10 has axon & adult head | conditional ts phenotype, suppressible by Scer\GAL4MS1075/htlλ.UAS

Nrgl10 has axon & adult head | conditional ts phenotype, suppressible by htlUAS.cMa/Scer\GAL4MS1075

Nrgl10 has axon & ocellus sensory structure | conditional ts phenotype, suppressible by EgfrE3

Nrgl10 has axon & mechanosensory neuron & adult head | conditional ts phenotype, suppressible by EgfrE3

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Nrgl10 is a non-enhancer of motor neuron phenotype of beat-IaC163/beat-Ia3, unc-58

NOT Suppressor of
Statement
Reference

Nrgl10 is a non-suppressor of motor neuron phenotype of beat-IaC163/beat-Ia3, unc-58

Additional Comments
Genetic Interactions
Statement
Reference

Nrgl10; unc-58 double mutants exhibit aberrant motoneuron crossing to the adjacent segment before the first branch point. The number of late defects is also substantially increased compared to both single mutants.

Nrgl10/Y; beat-IaC163/beat-Ia3 double mutants exhibit intersegmental nerve axon stalling prior to the first branch point.

Nrgl10/Y; unc-58, beat-IaC163/beat-Ia3 triple mutants exhibit severe defects in the intersegmental nerve crossing in the ventral muscle field.

Nrgl10/Y; unc-58/unc-58 double mutants do not exhibit any aCC or RP2 exit phenotypes.

Nrgl10/Y; beat-IaC163/beat-Ia3 double mutants do not exhibit any aCC or RP2 exit phenotypes.

The addition of a Nrgl10/Y background does not affect the unc-58, beat-IaC163/beat-Ia3 CNS exit failure seen in 10% of unc-58, beat-IaC163/beat-Ia3 hemisegments.

Removing one copy of eve in Nrgl10/Y mutants results in more severe intersegmental nerve guidance defects with a significant increase in axon stalling (from 3% to 21.2% upon the addition of eveΔRP2A).

The addition of htlScer\UAS.T:λ\cI-DD (when driven by Scer\GAL4MS1075) to Nrgl10 animals reduces the expressivity and penetrance of axon guidance defects. The frequency of axon guidance alterations are halved, though bristle mechanosensory (BM) axon extension defects are significantly enhanced. The addition of htlScer\UAS.cMa (when driven by Scer\GAL4MS1075) to Nrgl10 animals reduces the expressivity of axon guidance defects. The addition of htlAB42 to Nrgl10 animals shows a very mild enhancement of the axon guidance defects. The addition of Egfrunspecified to Nrgl10 animals shows an enhancement of the axon guidance defects. The addition of EgfrE3 or EgfrE1 to Nrgl10 animals shows a suppression of the axon guidance defects.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Nrgl10 complements the reduced female receptivity phenotype of Nrgibx at 18 and 25[o]C, but fails to complement this phenotype at 29[o]C. Nrgibx complements the lethality of Nrgl10 seen at 25[o]C.

Nrgl10 complements the reduced female receptivity phenotype of Nrg892 at 18 and 25[o]C, but fails to complement this phenotype at 29[o]C.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Complements: ibxM72.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (10)