FB2026_02 , released June 18, 2026
Allele: Dmel\neur1
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General Information
Symbol
Dmel\neur1
Species
D. melanogaster
Name
FlyBase ID
FBal0012940
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
neu9L119, neur9L119
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

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.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G9023617A

Reported nucleotide change:

G?A

Amino acid change:

G167E | neur-PA; G167E | neur-PB; G85E | neur-PC; G85E | neur-PD; G85E | neur-PE

Reported amino acid change:

G167E

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
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

neur1/neur11 stage 11 mutants exhibit an increase in the number of neuroblasts when compared to control embryos.

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.

Significantly fewer neur1 homozygous mutant germline stem cell clones survive compared to wild-type clones, indicating that neur is necessary for germline stem cell maintenance. Examination of the mutant germline stem cells reveals that they are phenotypically identical to wild-type.

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.);

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference

neur[+]/neur1 is an enhancer of visible phenotype of RalaEE1

NOT Enhancer of
Statement
Reference

neur1 is a non-enhancer of visible phenotype of RetMEN2B.GMR

NOT Suppressor of
Statement
Reference

neur1 is a non-suppressor of visible phenotype of RetMEN2B.GMR

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Enhancer of
Statement
Reference

neur[+]/neur1 is an enhancer of eye phenotype of RalaEE1

neur[+]/neur1 is an enhancer of eye photoreceptor cell & ommatidium | ectopic phenotype of lqfFDD9

neur[+]/neur1 is an enhancer of dorsal vessel wall cell | increased number phenotype of lqfARI

neur1 is an enhancer of phenotype of Brd1

neur1 is an enhancer of phenotype of Brd3

NOT Enhancer of
Statement
Reference

neur1 is a non-enhancer of eye phenotype of RetMEN2B.GMR

NOT Suppressor of
Statement
Reference

neur1 is a non-suppressor of eye phenotype of RetMEN2B.GMR

Additional Comments
Genetic Interactions
Statement
Reference

The rough eye phenotype of RalaEE1/Y adults is dominantly enhanced by neur1.

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.

Unlike lqfFDD9/lqfFDD9 animals, lqfFDD9/lqfFDD9; neur1/+ die as larvae.

Heterozygosity for neur1 increases the frequency of lqfARI embryos that show an excess cardioblast phenotype at 18oC.

No significant effect on the scaMSKF mutant phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

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.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Nusslein-Volhard, Wieschaus.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
References (38)