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General Information
Symbol
Dmel\NT141
Species
D. melanogaster
Name
FlyBase ID
FBal0240742
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
DNT141
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

The entire NT1 gene has been replaced by a w+* marker.

Insertion components
TI{TI}NT141
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 the CNS of homozygous NT141.Δ.w null mutant embryos, apoptosis levels are comparable to wild-type at stages 13/15, and there are no axon guidance defects. At embryonic stage 17, NT141.Δ.w, NT141.Δ.w/NT155.Δ.w and NT141.Δ.w/Df(3L)ED4342 null mutant embryos show a significant increase in apoptosis in the CNS.

NT141.Δ.w, NT141.Δ.w/NT155.Δ.w and NT141.Δ.w/Df(3L)ED4342 mutant embryos exhibit a significant increase in the incidence of misrouting phenotypes in ISNb/d and SN fascicles compared to wild-type, including effects in more than one projection per hemisegment (e.g. misrouting plus loss).

Loss of NT1 in NT141.Δ.w mutants affect ISNb/d projections more severely than SNa projections.

Targeted expression of NT1IR.pro.Scer\UAS in the CNS midline (under the control of Scer\GAL4sim.PS) in a NT141.Δ.w heterozygous background results in a significant increase in apoptosis throughout the CNS cortex compared to controls at embryonic stage 17.

Targeted expression of NT1IR.CK.Scer\UAS in the CNS midline (under the control of Scer\GAL4sim.PS) in a NT141.Δ.w heterozygous background results in a significant increase in apoptosis throughout the CNS cortex compared to controls at embryonic stage 17.

Targeted expression of NT1IR.CK.Scer\UAS in the muscle (under the control of Scer\GAL4how-24B) in a NT141.Δ.w heterozygous background results in a significant increase in the incidence of misrouting phenotypes in ISNb/d and SN fascicles compared to wild-type, including effects in more than one projection per hemisegment (e.g. misrouting plus loss).

In the CNS of homozygous NT141 null mutant embryos, apoptosis levels are comparable to wild-type at stages 13/15, and there are no axon guidance defects. At embryonic stage 17, NT141, NT141/NT155 and NT141/Df(3L)ED4342 null mutant embryos show a significant increase in apoptosis in the CNS.

NT141, NT141/NT155 and NT141/Df(3L)ED4342 mutant embryos exhibit a significant increase in the incidence of misrouting phenotypes in ISNb/d and SN fascicles compared to wild-type, including effects in more than one projection per hemisegment (e.g. misrouting plus loss).

Loss of NT1 in NT141 mutants affect ISNb/d projections more severely than SNa projections.

Targeted expression of NT1dsRNA.pro.Scer\UAS in the CNS midline (under the control of Scer\GAL4sim.PS) in a NT141 heterozygous background results in a significant increase in apoptosis throughout the CNS cortex compared to controls at embryonic stage 17.

Targeted expression of NT1dsRNA.CK.Scer\UAS in the CNS midline (under the control of Scer\GAL4sim.PS) in a NT141 heterozygous background results in a significant increase in apoptosis throughout the CNS cortex compared to controls at embryonic stage 17.

Targeted expression of NT1dsRNA.CK.Scer\UAS in the muscle (under the control of Scer\GAL4how-24B) in a NT141 heterozygous background results in a significant increase in the incidence of misrouting phenotypes in ISNb/d and SN fascicles compared to wild-type, including effects in more than one projection per hemisegment (e.g. misrouting plus loss).

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

NT141 has abnormal neuroanatomy phenotype, non-enhanceable by spz2

NT141 has increased cell death phenotype, non-enhanceable by spz2

Suppressed by
Statement
Reference

NT141 has viable phenotype, suppressible by spz5e03444

NOT suppressed by
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

NT141 is a non-enhancer of increased cell death phenotype of spz2

Suppressor of
Statement
Reference

NT141 is a suppressor of viable phenotype of spz5e03444

Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference

NT141 has larval segmental nerve phenotype, non-enhanceable by spz2

Enhancer of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

NT141, spz5e03444 double homozygosity leads to near lethality, which is rescued by Scer\GAL4elav.PU-driven expression of kek3UAS.mRFP(Unk), kek5UAS.mRFP(Unk) (leading to a small but significant increase in viability), kek2UAS.mRFP(Unk) or kek6UAS.mRFP(Unk) (leading to near full viability), but not kek1UAS.mRFP(Unk) or kek4UAS.mRFP(Unk).

DA1 and VA1d projection neuron dendrites and VA1d olfactory receptor neuron axons target normally in NT141 Df(3L)spz5AW18 double mutant flies.

The SNa axonal phenotype of spz2 NT141.Δ.w double-mutant embryos is epistatic to spz.

Loss of both NT1 and spz5 in spz5e03444 NT141.Δ.w double-mutant embryos results in an increase in apoptosis compared to each of the single mutants, revealing redundant or complementary functions in the control of neuronal survival.

Levels of apoptosis do not increase further in spz2 NT141.Δ.w double mutants (compared to spz2 mutants).

Whereas homozygous spz2 flies can eclose as adults, the NT141.Δ.w spz2 double mutants are completely lethal (100% penetrance).

Expression of spzact.Scer\UAS in NT141.Δ.w mutant embryos partially rescues apoptosis levels, but does not rescue the NT141.Δ.w mutant phenotype.

Viability is affected in NT141.Δ.w spz5e03444 double-mutants: in homozygosis, double mutant flies are viable (although some larval lethality, as well as when in trans over NT141.Δ.w Df(3L)Exel6092, is observed), but NT141.Δ.w spz5e03444/In(3LR)TM6B flies do not produce homozygous progeny at 18[o]C, suggesting unsuccessful larval competition.

The penetrance of ISNb/d targeting defects increases in spz5e03444 NT141.Δ.w / Df(3L)Exel6092 NT141.Δ.w double-mutant embryos, although not significantly.

The penetrance of both SNa and ISNb/d targeting defects increases in spz5e03444 NT141.Δ.w spz2, compared to the double or single mutants. In the triple mutants, misrouting phenotypes can be very dramatic, and there are cases of loss of all ISNb/d motor axons (not seen in single mutants). Misrouting of the transverse nerve (TN) can be very dramatic in triple mutants, although milder effects in this nerve occur with comparable penetrance in all genotypes (~10%). Misroutings of ISN are negligible in single and double mutants, but they increase and can be dramatic in triple-mutant embryos (12.7%).

NT141.Δ.w spz5e03444 / NT141.Δ.w Df(3L)Exel6092 double mutant flies display a range of behavioral phenotypes including: inability to estimate the location of a petri dish rim, falling off a petri dish rim, sluggishness, inability to climb, and wobbling.

The SNa axonal phenotype of spz2 NT141 double-mutant embryos is epistatic to spz.

Loss of both NT1 and spz5 in spz5e03444 NT141 double-mutant embryos results in an increase in apoptosis compared to each of the single mutants, revealing redundant or complementary functions in the control of neuronal survival.

Levels of apoptosis do not increase further in spz2 NT141 double mutants (compared to spz2 mutants).

Whereas homozygous spz2 flies can eclose as adults, the NT141 spz2 double mutants are completely lethal (100% penetrance).

Expression of spzact.Scer\UAS in NT141 mutant embryos partially rescues apoptosis levels, but does not rescue the NT141 mutant phenotype.

Viability is affected in NT141 spz5e03444 double-mutants: in homozygosis, double mutant flies are viable (although some larval lethality, as well as when in trans over NT141 Df(3L)Exel6092, is observed), but NT141 spz5e03444/In(3LR)TM6B flies do not produce homozygous progeny at 18[o]C, suggesting unsuccessful larval competition.

The penetrance of ISNb/d targeting defects increases in spz5e03444 NT141 / Df(3L)Exel6092 NT141 double-mutant embryos, although not significantly.

The penetrance of both SNa and ISNb/d targeting defects increases in spz5e03444 NT141 spz2, compared to the double or single mutants. In the triple mutants, misrouting phenotypes can be very dramatic, and there are cases of loss of all ISNb/d motor axons (not seen in single mutants). Misrouting of the transverse nerve (TN) can be very dramatic in triple mutants, although milder effects in this nerve occur with comparable penetrance in all genotypes (~10%). Misroutings of ISN are negligible in single and double mutants, but they increase and can be dramatic in triple-mutant embryos (12.7%).

NT141 spz5e03444 / NT141 Df(3L)Exel6092 double mutant flies display a range of behavioral phenotypes including: inability to estimate the location of a petri dish rim, falling off a petri dish rim, sluggishness, inability to climb, and wobbling.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of NT1Cysknot.Scer\UAS in all neurons (under the control of Scer\GAL4elav-C155) in embryos mutant for NT141.Δ.w leads to a significant reduction in apoptosis compared to NT141.Δ.w mutants.

Expression of NT1Cysknot.Scer\UAS in all neurons (under the control of Scer\GAL4elav-C155) in embryos mutant for NT141 leads to a significant reduction in apoptosis compared to NT141 mutants.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (6)