FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\neur11
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General Information
Symbol
Dmel\neur11
Species
D. melanogaster
Name
FlyBase ID
FBal0012950
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
neuIF65, neurIF65, neur1F65, neu11
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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

cuticle & macrochaeta | somatic clone

eye photoreceptor cell & ommatidium | ectopic | somatic clone

macrochaeta & mesothoracic tergum | somatic clone

thorax & chaeta | somatic clone

Detailed Description
Statement
Reference

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

Large neur11 clones in the larval notum show denser SOP rows, as compared to controls.

neur11 late stage 10 embryos exhibit an excess number of Asense-positive interstitial cell precursors, and present defects in posterior midgut remodeling, as shown by significantly fewer PGCs migrating through the posterior midgut epithelium, as compared to controls.

Homozygous intestinal stem cell clones contain few polyploid enterocytes.

Within neur11 clones, an apical actin-rich structure (ARS) is formed normally in all SOP progeny.

Homozygous intestinal stem cell (ISC) clones in the adult midgut either form tumours or differentiate into a single enterocyte.

Significantly fewer neur11 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.

neur11 clones in the adult notum are bald.

Ommatidia in neur11 homozygous clones in the adult eye contain extra photoreceptor cells.

The progeny of neur11 mutant pI cells produce no external sensory structures indicating that pIIa cells have been transformed into pIIb-like cells. Mitotic recombination of neur11/+ mutants, induced at 0-6 hours before puparium formation, produces flies with double-shaft bristles on the head, thorax and at the wing margin. This double-shaft phenotype appears to result from wild-type pIIb/neur11 mutant pIIa pairs because sensory organs composed of two mutant shaft cells (and no socket) with wild-type pIIb progeny cells are detected 20 hours after puparium formation. Reciprocally, a sheath-to-neuron transformation is observed in neur11 mutant pIIb/ wild-type pIIa pairs. neur11 mutant clones lead to the specification of a large excess of pI cells in the developing notum.

Mutants show no obvious mushroom body defect.

Homozygous somatic clones in the notum fail to differentiate the external components of sensory organs resulting in bald cuticle. Homozygous somatic clones in the sensory lineage can result in the transformation of the socket cell into a shaft cell. Homozygous somatic clones in the wing lead to either patches of anterior wing margin completely lacking in triple row bristles or triple row bristles with double shafts.

Flies carrying homozygous somatic clones in the eye die during pupal development - large necrotic patches are seen the eyes of these pupae by 45 hours after puparium formation. Their ommatidia are poorly defined, lenses are not properly secreted and all interommatidial bristle structures are missing. The arrangement and morphology of the rhabdomeres are severely disrupted in a cell autonomous fashion.

Mutant embryos show hypertrophy of the nervous system. neur11 embryos carrying neurT42.Scer\UAS.T:Hsap\MYC expressed under the control of Scer\GAL4ptc-559.1 have a greatly reduced nervous system.

Homozygous mutant embryos display sever hyperplasia to the central nervous system. Homozygous mutant clones give rise to a balding phenotype characterised by the absence of chaetae on the adult notum. When the pupal notum is examined, futsch expression reveals clusters of sensory organ precursors sometime containing up to four cells that differentiate to assume neural cell fates.

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 medial clusters expand across the midline.

Homozygous embryos have an increased number of cardiac precursor cells.

Thickened vein mutant.

Embryos exhibit few, if any, fused muscles. The unfused, birefringent fibres, may have a patterned arrangement. The birefringent is clearly correlated with the expansion of the CNS and PNS, and the loss of epidermis and the degree to which myoblast fusion occurs. Where myoblast fusion fails conspicuous clusters of mesodermal cells are formed and if epidermal territories are expanded cells in these clusters may be recruited to fusion.

Extreme neurogenic phenotype.

neur11 shows severe neural hypertrophy, a 6--9 fold increase in nau expressing cells per cluster relative to wild type. The clusters enlarge so much that they merge to form superclusters across the midline.

neur11 expression was modified by the presence of ASC loss-of-function mutations.

Severity of the phenotype is increased by duplication of Dl+ and decreased by triploidy for N.

Homozygous clones in the eye have a severely disturbed ommatidial pattern, visible as a scar in the eye surface. Ommatidia are larger than wild-type and interommatidial bristles are missing. Each ommatidium contains more retinula cells and fewer pigment cells than wild-type. Each ommatidium contains more receptor cells than normal, and may contain up to 13 receptor cells. Homozygous clones in the cuticle lack all bristles.

Extreme embryonic neurogenic phenotype. Only remaining epidermis is indicated by a patch of dorsal cuticle in which the posterior spiracles and a rudimentary anal plate are evident.

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

neur11 is an enhancer of visible phenotype of RetGMR.PR

NOT Enhancer of
Statement
Reference

neur11 is a non-enhancer of visible phenotype of RetMEN2B.GMR

neur11 is a non-enhancer of visible phenotype of RetMEN2A.GMR

Suppressor of
Statement
Reference

neur[+]/neur11 is a suppressor of visible | heat sensitive phenotype of HC2.hs

NOT Suppressor of
Statement
Reference

neur11 is a non-suppressor of visible phenotype of RetMEN2B.GMR

neur11 is a non-suppressor of visible phenotype of RetMEN2A.GMR

Phenotype Manifest In
Suppressed by
Enhancer of
Statement
Reference

neur[+]/neur11 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, fruNP0021

neur11 is an enhancer of eye phenotype of RetGMR.PR

neur11 is an enhancer of phenotype of Brd1

neur11 is an enhancer of phenotype of Brd3

NOT Enhancer of
Statement
Reference

neur11 is a non-enhancer of eye phenotype of RetMEN2B.GMR

neur11 is a non-enhancer of eye phenotype of RetMEN2A.GMR

Suppressor of
Statement
Reference

neur[+]/neur11 is a suppressor of wing vein | ectopic | heat sensitive phenotype of HC2.hs

neur[+]/neur11 is a suppressor of wing | heat sensitive phenotype of HC2.hs

NOT Suppressor of
Statement
Reference

neur11 is a non-suppressor of eye phenotype of RetMEN2B.GMR

neur11 is a non-suppressor of eye phenotype of RetMEN2A.GMR

neur11 is a non-suppressor of phenotype of Src42ASu(Raf)1-1

neur11 is a non-suppressor of phenotype of sno71e3

Other
Statement
Reference

Scer\GAL4sca-537.4, mib1UAS.Tag:polyHis,Tag:MYC, neur11 has macrochaeta & mesothoracic tergum | somatic clone phenotype

Additional Comments
Genetic Interactions
Statement
Reference

A neur11 heterozygous background enhances the rough eye phenotype related to fru isoform B, found upon expression of fruNP0021 under the control of Scer\GAL4GMR.PF.

Expression of mib1Scer\UAS.T:Zzzz\His6,T:Hsap\MYC under the control of Scer\GAL4sca-537.4 rescues bald neur11 clones back to a mild bristle tufting phenotype. Staining at the sensory precursor level shows that mib1Scer\UAS.T:Zzzz\His6,T:Hsap\MYC expression rescues pIIa specification in neur11 clones.

The number of photoreceptors per ommatidium in lqfFDD9/lqfFDD9 flies is increased still further by neur11/+.

Does not suppress the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.

There is no detectable dominant interaction with sno71e3.

Not capable of rescuing the lethality conferred NAx-E2/NAx-9 heterozygotes.

H2 reduces the severity of the phenotype of neur11 clones in the eye.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

The embryonic nervous system phenotype is partially rescued by neurScer\UAS.T:Hsap\MYC or neurScer\UAS.cYa when driven by Scer\GAL4ptc-559.1. Ventral cuticle is also restored.

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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (66)