Expressing JraJbz.UAS under the control of Scer\GAL4tey-5053A (together with Dicer-2, for efficient RNAI) does not provide protection against (injury-induced) Wallerian degeneration of third instar larval motoneurons.
Overexpression of JraJbz.Scer\UAS in combination with Scer\GAL4Scer\UAS.cHa driven by Scer\GAL4Tab2-201Y does not affect axon pruning.
Expression of JraJbz.Scer\UAS under the control of Scer\GAL4D42 in the presence of Scer\GAL80Cha.PK (to suppress expression in cholinergic neurons) results in a significant decrease in total dendritic length and in the number of dendritic branches in MN5 motorneurons.
Expression of JraJbz.Scer\UAS using Scer\GAL4ey-OK107 does not result in any gross axonal phenotypes.
Expression of JraJbz.Scer\UAS in the RP2 motor neurons (using the Scer\GAL4eve.RRK driver to drive expression of Scer\FLP1Scer\UAS.cUa which then induces clones of cells expressing Scer\GAL4Act.PU) results in a significant decrease in RP2 dendrite volume compared to controls.
Expression of JraJbz.Scer\UAS under the control of Scer\GAL4elav.PH in clones induced by FLP/FRT mediated recombination (to activate the Scer\GAL4elav.PH driver) results in a decrease in the number of type 1b boutons at muscle 13 compared to wild type.
Expression of JrabZIP.Scer\UAS under the control of Scer\GAL4pnr-MD237 results in a mild cleft thorax phenotype.
Expression of JraJbz.Scer\UAS under the control of Scer\GAL4elav-C155 results in an approximately 25% reduction in EJC amplitude (synaptic strength) and bouton number at the larval neuromuscular junction. mEJC amplitude is not significantly altered.
Scer\GAL4-mediated expression in the eye imaginal disc interferes with proper eye development.
Scer\GAL4C-765, Scer\GAL469B and Scer\GAL4hs.PB-mediated expression causes defects in head and dorsal cuticle. Scer\GAL4C-765 induces predominantly an anterior open-like phenotype and Scer\GAL469B and Scer\GAL4hs.PB lead to phenotypes that progressively affect the entire dorsal cuticle. No defects in posterior structures and filzkorper are observed.
Causes no effect on copper cell development, when expression is driven by Scer\GAL448Y.
JraJbz.UAS, Scer\GAL4elav-C155 has abnormal neuroanatomy phenotype, suppressible by pucE69
JraJbz.UAS, Scer\GAL4elav-C155 has abnormal neurophysiology phenotype, suppressible by pucE69
JraJbz.UAS, Scer\GAL4ey-OK107 is an enhancer of abnormal neuroanatomy phenotype of Scer\GAL4ey-OK107, bskGD10555
Scer\GAL4tey-5053A/JraJbz.UAS is a suppressor | partially of abnormal neuroanatomy | recessive | third instar larval stage | conditional phenotype of rawdcp-1
JraJbz.UAS, Scer\GAL4ptc-559.1 is a suppressor | partially of abnormal cell migration | third instar larval stage phenotype of Scer\GAL4ptc-559.1, pucGD1515
Scer\GAL4elav.PU/JraJbz.UAS is a suppressor | partially of abnormal neuroanatomy | maternal effect | larval stage phenotype of SkpAGD65
Scer\GAL4BG380/JraJbz.UAS is a non-suppressor of abnormal neurophysiology phenotype of hiwND8
JraJbz.UAS, Scer\GAL4tey-5053A, rawdcp-1 has abnormal neuroanatomy | third instar larval stage phenotype
JraJbz.UAS, Scer\GAL4ey-OK107, kayFbz.UAS has abnormal neuroanatomy phenotype
JraJbz.UAS, Mnn1UAS.cCa, Scer\GAL4how-24B has lethal | pupal stage P7 phenotype
JraJbz.UAS, Scer\GAL4pnr-MD237 has adult thorax phenotype, enhanceable by Mnn1UAS.cCa, Scer\GAL4pnr-MD237
JraJbz.UAS, Scer\GAL4elav-C155 has bouton phenotype, suppressible by pucE69
JraJbz.UAS, Scer\GAL4elav-C155 has neuromuscular junction | larval stage phenotype, suppressible by pucE69
JraJbz.UAS, Scer\GAL4ey-OK107 is an enhancer of Kenyon cell phenotype of Scer\GAL4ey-OK107, bskGD10555
JraJbz.UAS, Scer\GAL4ey-OK107 is an enhancer of axon phenotype of Scer\GAL4ey-OK107, bskGD10555
JraJbz.UAS, Scer\GAL4pnr-MD237 is an enhancer of adult thorax phenotype of Mnn1UAS.cCa, Scer\GAL4pnr-MD237
Scer\GAL4tey-5053A/JraJbz.UAS is a suppressor | partially of axon | third instar larval stage | conditional phenotype of rawdcp-1
Scer\GAL4tey-5053A/JraJbz.UAS is a suppressor | partially of embryonic/larval motor neuron | third instar larval stage | conditional phenotype of rawdcp-1
JraJbz.UAS, Scer\GAL4ptc-559.1 is a suppressor | partially of anterior-posterior compartment boundary of the wing disc | third instar larval stage phenotype of Scer\GAL4ptc-559.1, pucGD1515
Scer\GAL4elav.PU/JraJbz.UAS is a suppressor | partially of NMJ bouton | maternal effect | larval stage phenotype of SkpAGD65
Scer\GAL4elav.PU/JraJbz.UAS is a suppressor | partially of embryonic/larval neuromuscular junction | maternal effect | larval stage phenotype of SkpAGD65
Scer\GAL4BG380/JraJbz.UAS is a non-suppressor of neuromuscular junction phenotype of hiwND8
Scer\GAL4BG380/JraJbz.UAS is a non-suppressor of bouton phenotype of hiwND8
JraJbz.UAS, Scer\GAL4tey-5053A, rawdcp-1 has axon | third instar larval stage phenotype
JraJbz.UAS, Scer\GAL4ey-OK107, kayFbz.UAS has axon phenotype
JraJbz.UAS, Scer\GAL4ey-OK107, kayFbz.UAS has Kenyon cell phenotype
rawdcp-1 homozygotes show protection against (injury-induced) Wallerian degeneration in third instar larval motor neurons, which is considerably suppressed by the expression of JraJbz.UAS under the control of Scer\GAL4tey-5053A; in these double mutants, injured axons exhibit severely decreased new growth/sprouting compared to controls.
The synaptic overgrowth phenotype (increase in bouton number) seen at the neuromuscular junction in larvae derived from homozygous SkpAGD65 females is partially suppressed by expression of JraJbz.Scer\UAS under the control of Scer\GAL4elav.PU.
The reduction in total dendritic length and in the number of dendritic branches which is seen in MN5 motorneurons in animals expressing JraJbz.Scer\UAS under the control of Scer\GAL4D42 in the presence of Scer\GAL80Cha.PK (to suppress expression in cholinergic neurons) is not altered if the flies are also simultaneously co-expressing both ShDN.EKI.Scer\UAS and eagDN.EKI.Scer\UAS.
Co-expression of kayFbz.Scer\UAS and JraJbz.Scer\UAS results in axon degeneration phenotypes.
Co-expression of two copies of JraJbz.Scer\UAS strongly enhances the axonal defects seen in Scer\GAL4ey-OK107, bskGD10555 animals.
The border follicle cell migration defects that are seen in flies co-expressing both PvrDN.Scer\UAS and hepAct.Scer\UAS under the control of Scer\GAL4slbo.2.6 are not strongly affected by the co-expression of JraJbz.Scer\UAS.
The cleft thorax phenotype of flies that express either Mnn1Scer\UAS.cCa or JrabZIP.Scer\UAS under the control of Scer\GAL4pnr-MD237 is enhanced when Mnn1Scer\UAS.cCa and JrabZIP.Scer\UAS are expressed together by Scer\GAL4pnr-MD237. Further, flies that coexpress Mnn1Scer\UAS.cCa and JrabZIP.Scer\UAS under the control of Scer\GAL4how-24B are lethal at pupal stage P7, which is earlier than the pharate adult lethality of Scer\GAL4how-24B>Mnn1Scer\UAS.cCa flies.
Expression of JraJbz.Scer\UAS, under the control of Scer\GAL4BG380 does not suppress the hiwND8 synaptic phenotype.
Protein acts as a dominant negative as the bZIP domain is able to dimerize and bind DNA without being able to stimulate transcription.