increased cell death | embryonic stage 17 (with NT1RNAi.CK.UAS), with Scer\GAL4sim.PS
increased cell death | embryonic stage 17 (with NT1RNAi.pro.UAS), with Scer\GAL4sim.PS
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).
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).
NT141, spz2 has abnormal neuroanatomy phenotype, enhanceable by spz5e03444
NT141 has abnormal neuroanatomy phenotype, enhanceable by spz2/spz5e03444
NT141, spz5e03444 has abnormal neuroanatomy phenotype, enhanceable by spz2
Df(3L)ED4342/NT141 has abnormal neuroanatomy phenotype, enhanceable by spz5e03444
NT141 has abnormal neuroanatomy phenotype, non-enhanceable by spz2
NT141 has increased cell death phenotype, non-enhanceable by spz2
NT141, spz5e03444 has lethal phenotype, suppressible by Scer\GAL4elav.PU/kek2UAS.mRFP(Unk)
NT141, spz5e03444 has lethal phenotype, suppressible by Scer\GAL4elav.PU/kek3UAS.mRFP(Unk)
NT141, spz5e03444 has lethal phenotype, suppressible by kek5UAS.mRFP(Unk)/Scer\GAL4elav.PU
NT141, spz5e03444 has lethal phenotype, suppressible by Scer\GAL4elav.PU/kek6UAS.mRFP(Unk)
NT141, spz5e03444 has some die during embryonic stage | heat sensitive phenotype, suppressible by Toll-7C993Y.UAS.Tag:FLAG/Scer\GAL4elav-C155
NT141, spz5e03444 has some die during embryonic stage | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/Toll-7ΔLRR.UAS.Tag:HA
NT141, spz5e03444 has some die during embryonic stage | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/Tl10b.UAS.cYa
NT141, Toll-626 has some die during embryonic stage | heat sensitive phenotype, suppressible by Toll-7C993Y.UAS.Tag:FLAG/Scer\GAL4Toll-7
NT141, Toll-626 has some die during embryonic stage | heat sensitive phenotype, suppressible by Scer\GAL4Toll-7/Toll-6C1020Y.UAS.Tag:FLAG
NT141, spz5e03444 has some die during embryonic stage | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/Toll-6ΔLRR.UAS.Tag:HA
NT141 has increased cell death phenotype, suppressible by Scer\GAL4elav-C155/spzact.UAS
NT141, spz5e03444 has lethal phenotype, non-suppressible by Scer\GAL4elav.PU/kek1UAS.mRFP(Unk)
NT141, spz5e03444 has lethal phenotype, non-suppressible by Scer\GAL4elav.PU/kek4UAS.mRFP(Unk)
NT141 is an enhancer of abnormal neuroanatomy phenotype of spz5e03444, spz2
NT141/spz5e03444 is an enhancer of abnormal neuroanatomy phenotype of spz2
spz2/NT141 is an enhancer of abnormal neuroanatomy phenotype of spz5e03444
Df(3L)ED4342/NT141 is an enhancer of abnormal neuroanatomy phenotype of spz5e03444
NT141 is a non-enhancer of increased cell death phenotype of spz2
NT141, spz5e03444 has lethal phenotype
NT141, Toll-7P114 has some die during embryonic stage | heat sensitive phenotype
NT141, spz5e03444 has some die during embryonic stage | heat sensitive phenotype
Df(3L)Exel6092, NT141 has some die during embryonic stage | heat sensitive phenotype
NT141, Toll-626 has some die during embryonic stage | heat sensitive phenotype
NT141, spz5e03444, spz2 has abnormal locomotor rhythm phenotype
Df(3L)ED4342/NT141, spz5e03444, spz2 has abnormal locomotor rhythm phenotype
NT141, spz2 has larval segmental nerve phenotype, enhanceable by spz5e03444
NT141, spz2 has larval transverse nerve phenotype, enhanceable by spz5e03444
NT141 has larval intersegmental nerve branch ISNb of A1-7 phenotype, enhanceable by spz2/spz5e03444
NT141 has larval intersegmental nerve branch ISNd of A1-7 phenotype, enhanceable by spz2/spz5e03444
NT141 has larval segmental nerve branch SNa of A1-7 phenotype, enhanceable by spz2/spz5e03444
NT141 has larval segmental nerve phenotype, enhanceable by spz2/spz5e03444
NT141 has larval transverse nerve phenotype, enhanceable by spz2/spz5e03444
NT141, spz5e03444 has larval intersegmental nerve branch ISNb of A1-7 phenotype, enhanceable by spz2
NT141, spz5e03444 has larval intersegmental nerve branch ISNd of A1-7 phenotype, enhanceable by spz2
NT141, spz5e03444 has larval segmental nerve phenotype, enhanceable by spz2
NT141, spz5e03444 has larval transverse nerve phenotype, enhanceable by spz2
Df(3L)ED4342/NT141 has larval intersegmental nerve branch ISNb of A1-7 phenotype, enhanceable by spz5e03444
Df(3L)ED4342/NT141 has larval intersegmental nerve branch ISNd of A1-7 phenotype, enhanceable by spz5e03444
Df(3L)ED4342/NT141 has larval segmental nerve phenotype, enhanceable by spz5e03444
NT141, spz2 has larval intersegmental nerve branch ISNb of A1-7 phenotype, enhanceable by spz5e03444
NT141, spz2 has larval intersegmental nerve branch ISNd of A1-7 phenotype, enhanceable by spz5e03444
NT141 has larval segmental nerve phenotype, non-enhanceable by spz2
NT141 is an enhancer of larval intersegmental nerve branch ISNb of A1-7 phenotype of spz5e03444, spz2
NT141 is an enhancer of larval intersegmental nerve branch ISNd of A1-7 phenotype of spz5e03444, spz2
NT141 is an enhancer of larval segmental nerve phenotype of spz5e03444, spz2
NT141 is an enhancer of larval transverse nerve phenotype of spz5e03444, spz2
NT141/spz5e03444 is an enhancer of larval intersegmental nerve branch ISNb of A1-7 phenotype of spz2
NT141/spz5e03444 is an enhancer of larval intersegmental nerve branch ISNd of A1-7 phenotype of spz2
NT141/spz5e03444 is an enhancer of larval segmental nerve branch SNa of A1-7 phenotype of spz2
NT141/spz5e03444 is an enhancer of larval segmental nerve phenotype of spz2
NT141/spz5e03444 is an enhancer of larval transverse nerve phenotype of spz2
spz2/NT141 is an enhancer of larval intersegmental nerve branch ISNb of A1-7 phenotype of spz5e03444
spz2/NT141 is an enhancer of larval intersegmental nerve branch ISNd of A1-7 phenotype of spz5e03444
spz2/NT141 is an enhancer of larval segmental nerve branch SNa of A1-7 phenotype of spz5e03444
spz2/NT141 is an enhancer of larval segmental nerve phenotype of spz5e03444
spz2/NT141 is an enhancer of larval transverse nerve phenotype of spz5e03444
Df(3L)ED4342/NT141 is an enhancer of larval intersegmental nerve branch ISNb of A1-7 phenotype of spz5e03444
Df(3L)ED4342/NT141 is an enhancer of larval intersegmental nerve branch ISNd of A1-7 phenotype of spz5e03444
Df(3L)ED4342/NT141 is an enhancer of larval segmental nerve phenotype of spz5e03444
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 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.
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.
NT141 is rescued by Scer\GAL4elav-C155/NT1Cysknot.UAS
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.