Carries a G-to-A transition in the second exon (residue numbering is in reference to the PA isoform of neur) resulting in a Gly167 to Glu substitution.
G9023617A
G?A
G167E | neur-PA; G167E | neur-PB; G85E | neur-PC; G85E | neur-PD; G85E | neur-PE
G167E
neuron & eye | supernumerary | somatic clone
neur1 heterozygotes exhibit learning and 9-minute memory abilities that appear identical to wild-type controls. However, these animals display significantly reduced 260-minute memory.
neur1 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 11% of SOP positions scored. Approximately 33.5% of SOP positions display between four and eight ectopic SOPs, while approximately 48% exhibit between one and four SOPs, with only 7.5% exhibiting one SOP, as in wild-type.
The presence of neur1 mutant cells within an ommatidium is often associated with changes in the number of photoreceptor cells: ommatidia with too many or too few photoreceptors are both observed. Less often, ommatidia containing one or more neur1 cells differentiate 8 photoreceptor cells in the normal arrangement. Ommatidia almost never develop normally with a neur1 R8 cell, and only rarely develop normally with a neur1 R3 cell - when the R3 cell is neur1 mutant, symmetrical ommatidia often develop, with two R3 cells in place of R3/R4. Ommatidia develop normally when the R7 is neur1 mutant. R1 and R6 are never both mutant for neur1 in normal ommatidia.
The average number of crystal cells per embryo is reduced in homozygous stage 13-14 embryos compared to wild type.
Homozygous mutant somatic clonesare neuorgenic in the eye.
Sensory organ precursors (SOPs) at the prospective wing margin of third instar larval wing discs are lost in neur1 somatic clones, except in cases where a cell within the clone abuts wild-type wing margin cells. There may be some non-autonomous effect of these clones on SOPs: 60% of the clones have wild-type (WT) SOPs next to neur1 mutant non-SOPs; 18% of clones have WT non-SOPs next to neur1 mutant SOPs; 23% have adjacent WT and neur1 mutant SOPs. This is similar to the results obtained with DlRevF10 somatic clones.
The number of cells in the nau-expressing muscle precursor clusters is increased compared to wild-type in homozygous embryos and in homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic function).
The number of peripheral, exit and dorsal roof glia in mutant embryos is higher than in wild-type embryos.
ac protein distribution in neur1 embryos show ac expression is not restricted to a single cell of an ectodermal cell cluster, instead most cells of the cluster retain ac expression at a high level, enlarge, delaminate and become neuroblasts.
Extreme embryonic neurogenic phenotype.
strong allele embryonic lethal hyperplasia of neural components at the expense of epidermal components as seen in other neurogenic lethal mutations (N, bib, mam, etc.);
neur1 is a non-enhancer of visible phenotype of RetMEN2B.GMR
neur1 is a non-suppressor of visible phenotype of RetMEN2B.GMR
neur1 has sensory mother cell | ectopic phenotype, enhanceable by mib1EY09780
neur1 has sensory mother cell | ectopic | somatic clone phenotype, enhanceable by DeltaRevF10
neur1 has sensory mother cell | ectopic | somatic clone phenotype, enhanceable by SerRX106
neur1 has sensory mother cell | ectopic | somatic clone phenotype, enhanceable by mib1EY09780
neur1 is an enhancer of sensory mother cell | third instar larval stage | ectopic | somatic clone phenotype of DeltaRevF10
neur[+]/neur1 is an enhancer of dorsal vessel wall cell | increased number phenotype of lqfARI
neur1 is a non-enhancer of eye phenotype of RetMEN2B.GMR
neur1 is a non-suppressor of eye phenotype of RetMEN2B.GMR
neur1 DlRevF10 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 50% of SOP positions scored. Approximately 35% of SOP positions display between four and eight ectopic SOPs, while approximately 15% exhibit between one and four SOPs. No SOP positions appeared wild-type. Therefore neur enhances the Dl lateral inhibition phenotype. neur1 SerRX106 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 33.5% of SOP positions scored. Approximately 47% of SOP positions display between four and eight ectopic SOPs, while approximately 19.5% exhibit between one and four SOPs. No SOP positions appeared wild-type. Therefore neur enhances the Ser lateral inhibition phenotype. mib1EY09780 neur1 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 82.5% of SOP positions scored. Approximately 17.5% of SOP positions display between four and eight ectopic SOPs. No wild-type SOPs are found. Induction of neur1 mutant clones in a homozygous mib1EY09780 background results in a large number of ectopic sensory organ precursors.
No significant effect on the scaMSKF mutant phenotype.
neur1 is rescued by Scer\GAL4c747/neurUAS.cPa
Expression of neurScer\UAS.cPa under the control of Scer\GAL4c747 fully rescues 260-minute memory after conditioned and unconditioned stimuli pairings in neur1 mutants.
Nusslein-Volhard, Wieschaus.