FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Nrg849
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General Information
Symbol
Dmel\Nrg849
Species
D. melanogaster
Name
FlyBase ID
FBal0001576
Feature type
allele
Associated gene
Dmel\Nrg
Associated Insertion(s)
Carried in Construct
Also Known As
ceb1, ceb849
Key Links
Genomic Maps

Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
ethyl methanesulfonate
Progenitor genotype
Cytology
Description

Amino acid replacement: S213L.

(Godenschwege et al., 2006)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
X:8,545,284..8,545,284 [+]
Nucleotide change:

C8545284T

Amino acid change:

S213L | Nrg-PA; S213L | Nrg-PB; S213L | Nrg-PC; S213L | Nrg-PD; S213L | Nrg-PE; S213L | Nrg-PF; S213L | Nrg-PG; S213L | Nrg-PH; S213L | Nrg-PI

Reported amino acid change:

S213L

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Godenschwege et al., 2006)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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

      abnormal courtship behavior | female (with NrgG0099)

      (Carhan et al., 2005)

      abnormal courtship behavior | female (with NrgG0413)

      (Carhan et al., 2005)

      abnormal courtship behavior | female (with NrgG0488b)

      (Carhan et al., 2005)

      abnormal courtship behavior | female (with Nrgl4)

      (Carhan et al., 2005)

      abnormal courtship behavior | female | heat sensitive (with Nrgl10)

      (Carhan et al., 2005)

      abnormal courtship behavior | male

      (Carhan et al., 2005)

      abnormal locomotor behavior | larval stage | recessive

      (Varnam et al., 1996)

      abnormal memory

      (Liu et al., 2006)

      abnormal neuroanatomy

      (Godenschwege et al., 2006)

      abnormal neuroanatomy | adult stage

      (Clements et al., 2021, Kudumala et al., 2013)

      abnormal neuroanatomy | adult stage (with Nrg892)

      (Clements et al., 2021)

      abnormal neuroanatomy | adult stage (with NrgG00305)

      (Clements et al., 2021)

      abnormal neuroanatomy | adult stage (with Nrgl4)

      (Clements et al., 2021)

      abnormal neuroanatomy | adult stage (with Nrgl10)

      (Clements et al., 2021)

      abnormal neuroanatomy | P-stage

      (Clements et al., 2021)

      abnormal neurophysiology

      (Godenschwege et al., 2006)

      abnormal neurophysiology, with Nrg180.UAS, Scer\GAL4c17

      (Godenschwege et al., 2006)

      abnormal neurophysiology, with Nrg180.UAS, Scer\GAL4shakB.lethal.4.1

      (Godenschwege et al., 2006)

      abnormal neurophysiology, with Nrg180.UAS, Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      abnormal neurophysiology, with NrgGPI.UAS, Scer\GAL4c17

      (Godenschwege et al., 2006)

      abnormal neurophysiology, with NrgGPI.UAS, Scer\GAL4shakB.lethal.4.1

      (Godenschwege et al., 2006)

      abnormal neurophysiology, with NrgGPI.UAS, Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      abnormal oxidative stress response | adult stage

      (Clements et al., 2021)

      abnormal starvation stress response | adult stage

      (Clements et al., 2021)

      abnormal thermotaxis

      (Hong et al., 2008)

      viable

      (Clements et al., 2021)
      Phenotype Manifest In

      adult central complex

      (de Belle and Heisenberg, 1996, Strauss and Heisenberg, 1993)

      adult insulin secreting cell of pars intercerebralis

      (Clements et al., 2021)

      adult insulin secreting cell of pars intercerebralis (with Nrg892)

      (Clements et al., 2021)

      adult insulin secreting cell of pars intercerebralis (with NrgG00305)

      (Clements et al., 2021)

      adult insulin secreting cell of pars intercerebralis (with Nrgl4)

      (Clements et al., 2021)

      adult insulin secreting cell of pars intercerebralis (with Nrgl10)

      (Clements et al., 2021)

      adult mushroom body

      (de Belle and Heisenberg, 1996, Strauss and Heisenberg, 1993)

      calyx of adult mushroom body

      (Walcourt and Nash, 2000, de Belle and Heisenberg, 1996)

      ellipsoid body

      (Walcourt and Nash, 2000, de Belle and Heisenberg, 1996)

      fan-shaped body

      (Walcourt and Nash, 2000, de Belle and Heisenberg, 1996)

      giant fiber neuron

      (Godenschwege et al., 2006)

      giant fiber neuron | adult stage

      (Kudumala et al., 2013)

      insulin secreting cell of pars intercerebralis | P-stage

      (Clements et al., 2021)

      Kenyon cell

      (de Belle and Heisenberg, 1996, Strauss and Heisenberg, 1993)

      lobe system of adult mushroom body

      (de Belle and Heisenberg, 1996)

      medial lobe of adult mushroom body

      (Walcourt and Nash, 2000)

      mitochondrion & synapse

      (Godenschwege et al., 2006)

      motor neuron

      (Godenschwege et al., 2006)

      mushroom body vertical lobe

      (Walcourt and Nash, 2000)

      neurite | adult stage | ectopic

      (Clements et al., 2021)

      neurite | adult stage | ectopic (with Nrg892)

      (Clements et al., 2021)

      neurite | adult stage | ectopic (with NrgG00305)

      (Clements et al., 2021)

      neurite | adult stage | ectopic (with Nrgl4)

      (Clements et al., 2021)

      neurite | adult stage | ectopic (with Nrgl10)

      (Clements et al., 2021)

      neurite | P-stage | ectopic

      (Clements et al., 2021)

      synapse

      (Godenschwege et al., 2006)
      Detailed Description
      Statement
      Reference

      In Nrg849 mutants, one or both giant fibre neurons (GFs) are stalled in the suboesophageal ganglion of the brain with a penetrance of approximately 30%. The remaining GFs, once they have exited the brain, continue to grow to the synaptic target area.

      (Kudumala et al., 2013)

      Nrg849 mutant flies show abnormal temperature preference behavior.

      (Hong et al., 2008)

      Nrg849 mutants display a variety of synaptic defects. The tergo-trochanteral motor neuron (TTMn), is absent in 23% of cases and severely weakened in 61% of cases, while the dorsal longitudinal motor neuron (DLMn) response to the giant synapse is always present, although occasionally weakened. No response could be recorded from either the TTMn or the DLMn in approximately 14% of Nrg849 mutant animals.

      In approximately 83% of Nrg849 mutants, axons reach the target area in the second thoracic neuromere and exhibit a synaptic terminal (73%). Although the giant synapse-TTMn (tergo-trochanter motor neuron) connection is disrupted in Nrg849 mutants, in about 33% of flies the presynaptic terminals appear to be morphologically normal at the light-microscope level. However, some synaptic terminals do not grow to a normal diameter (approximately 43%) and a few fail to extend their presynaptic terminal laterally (approximately 10%). Finally, a small number never reach the target because of pathfinding errors in the brain (approximately 17%). All giant fibers stall in a similar position in the suboesophangeal ganglion. Once the giant fibers exit the brain, no guidance defects are found in the first thoracic neuromere, and all giant fibers reach the target area in the second thoracic neuromere.

      Only 49% of the giant fibers in Nrg849 specimens reveal Lucifer Yellow dye coupling between the giant fiber and the TTMn in comparison to 95% of control specimens with trans-synaptic fills. In those specimens with dye coupling and a physiologically mutant TTMn response, the trans-synaptic fills often appear much weaker in comparison to those in adults with a wild-type TTMn response. This implies the presence of gap junctions in half of the specimens but suggests that the electrical synapse is weakened.

      Nrg849 mutants exhibit ultrastructural defects in synaptic terminals, while not in axons. The presynaptic terminals of the giant fiber in wild-type specimens are crowded with synaptic vesicles, pleiomorphic vesicles, and tubulo-membranous structures. In contrast, the presynaptic terminal in Nrg849 mutant specimens appears 'empty', with very few vesicles or vacuoles. Nrg849 mutants exhibit an average of 3 vesicles per 0.25Ï…m2 around the T bar compared to 19 vesicles per 0.25Ï…m2 in the wild-type. This reduction in number of the various membranous vesicles and organelles is not only restricted to the active zones surrounding the T bars but is observed throughout the GF-TTMn contact region. Significantly fewer mitochondria (0.16 mitochondria per Ï…m2) are observed at the presynaptic terminal of Nrg849 compared to wild-type (0.65 mitochondria per Ï…m2). In addition, these mitochondria appear to be much farther away from the contact region. In contrast, no difference is observed between Nrg849 mutants and wild-type mitochondrial levels in the axons.

      Microtubules, observed in wild-type synaptic terminals (at a density of 4.59 microtubules per Ï…m2), are almost completely absent from Nrg849 mutants (0.14 microtubules per Ï…m2). In contrast, no difference is observed in microtubule density in the axons between Nrg849 mutants and wild-type controls.

      Presynaptic T bars and postsynaptic densities are observed in wild-type and mutant individuals. On average slightly fewer T bars per Ï…m contact length are found in Nrg849 mutants (0.36 T bars/;Ï…m2) compared to the wild-type (0.43 T bars/;Ï…m2), although the difference is not significant.

      (Godenschwege et al., 2006)

      Mutants have impaired visual pattern memory.

      (Liu et al., 2006)

      Homozygous, Nrg849/Nrgl7 and Nrg849/Nrg892 females show normal sexual receptivity when mated to wild-type males.

      Nrgl4/Nrg849, NrgG0099/Nrg849, NrgG0413/Nrg849 and NrgG0488b/Nrg849 females show reduced sexual receptivity compared to wild-type controls when mated to wild-type males.

      Nrgl10/Nrg849 females show normal sexual receptivity at 18 and 25[o]C, but show reduced receptivity at 29[o]C when mated to wild-type males.

      Homozygous males show defects in courtship behaviour relative to wild-type controls when mated to wild-type females. The mean latency is not significantly different from wild type, but they show significantly extended mating speeds. Once they are courting a female, the mutant males tend to have more breaks in their courtship than normal.

      (Carhan et al., 2005)

      Mutant adults have split fan-shaped and ellipsoid bodies in the brain and lack vertical and medial lobes. The calyces are misshapen and are often divided into multiple lobes, but their volume is not greatly enlarged. Long and short latency responses are indistinguishable from wild-type flies in both the DLM (flight) and TTM (jump) muscles. EC50 values (the concentration at which half of the long latency responses are expected to fail) for halothane and enflurane for mutant flies are indistinguishable from the EC50 values of Canton-S controls.

      (Walcourt and Nash, 2000)

      Homozygous larvae show reduced locomotor behaviour (shorter path lengths) on agar (non-foraging surface) and yeast (foraging surface) compared to controls. Larvae are slightly faster than controls in a roll over test.

      (Varnam et al., 1996)

      Flies have a number of brain defects, the exact phenotype depending on the genetic background. In the original genetic background in which it was induced, Nrg849 produces the following phenotype; the calyx is enlarged and misshapen, Kenyon cell axons form an extra 'lateral calyx', the peduncle and lobes are absent or thin, the ellipsoid body is open ventrally, flattened or divided and the fan-shaped body is absent in most flies. When placed in a Canton S background, the Nrg849 phenotype is altered, and the calyx becomes larger and more misshapen than in the original genetic background, the peduncle and lobes are absent, and the central complex is more disturbed.

      (de Belle and Heisenberg, 1996)

      Abnormalities in central body and mushroom body. About 400 Kenyon cell fibers miss the fiber bundle of pedicle, forming an extra lobe on lateral side of calyx. Ellipsoid body abnormal, being divided into 2 parts along the midline, or opening ventrally.

      (Strauss and Heisenberg, 1993)

      Extra lobe, in adult brain, of approximately 400 coiled Kenyon-cell fibers next to calyx of mushroom bodies; olfactory learning in adults slightly reduced; memory is normal.

      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressed by
      NOT suppressed by
      Phenotype Manifest In
      Suppressed by
      NOT suppressed by
      Statement
      Reference

      Nrg849 has giant fiber neuron | adult stage phenotype, non-suppressible by Hsap\L1CAMC264Y.UAS/Scer\GAL4shot-OK307

      (Kudumala et al., 2013)

      Nrg849 has giant fiber neuron | adult stage phenotype, non-suppressible by Hsap\L1CAMR184Q.UAS/Scer\GAL4shot-OK307

      (Kudumala et al., 2013)

      Nrg849 has giant fiber neuron | adult stage phenotype, non-suppressible by Hsap\L1CAM4A.UAS/Scer\GAL4shot-OK307

      (Kudumala et al., 2013)

      Nrg849 has giant fiber neuron | adult stage phenotype, non-suppressible by Hsap\L1CAMH210Q.UAS/Scer\GAL4shot-OK307

      (Kudumala et al., 2013)

      Nrg849 has giant fiber neuron phenotype, non-suppressible by Fas2UAS.cLa/Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      Nrg849 has synapse phenotype, non-suppressible by Fas2UAS.cLa/Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      Nrg849 has giant fiber neuron phenotype, non-suppressible by Hsap\L1CAMH210Q.UAS/Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      Nrg849 has synapse phenotype, non-suppressible by Hsap\L1CAMH210Q.UAS/Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      Nrg849 has giant fiber neuron phenotype, non-suppressible by Scer\GAL4shot-OK307/Hsap\NCAM1UAS.cGa

      (Godenschwege et al., 2006)

      Nrg849 has synapse phenotype, non-suppressible by Scer\GAL4shot-OK307/Hsap\NCAM1UAS.cGa

      (Godenschwege et al., 2006)

      Nrg849 has giant fiber neuron phenotype, non-suppressible by Rnor\NrcamUAS.cGa/Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      Nrg849 has synapse phenotype, non-suppressible by Rnor\NrcamUAS.cGa/Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      Nrg849 has giant fiber neuron phenotype, non-suppressible by Ggal\NFASCUAS.cGa/Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)

      Nrg849 has synapse phenotype, non-suppressible by Ggal\NFASCUAS.cGa/Scer\GAL4shot-OK307

      (Godenschwege et al., 2006)
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Expression of Fas2Scer\UAS.cLa pre- and post-synaptically, under the control of Scer\GAL4A307 in a Nrg849 heterozygous background fails to suppresses the Nrg849 giant synapse physiological phenotype.

      (Godenschwege et al., 2006)
      Xenogenetic Interactions
      Statement
      Reference

      Expression of Hsap\L1CAMRSLE-.Scer\UAS under the control of Scer\GAL4OK307 significantly suppresses the giant fibre axon guidance defects seen in Nrg849 mutant flies.

      Expression of Hsap\L1CAML120V.Scer\UAS significantly suppresses the giant fibre axon guidance defects seen in Nrg849 mutant flies.

      Expression of Hsap\L1CAMH38.Scer\UAS significantly suppresses the giant fibre axon guidance defects seen in Nrg849 mutant flies.

      Expression of Hsap\L1CAMC264Y.Scer\UAS does not suppress the giant fibre axon guidance defects seen in Nrg849 mutant flies.

      Expression of Hsap\L1CAMH210Q.Scer\UAS does not suppress the giant fibre axon guidance defects seen in Nrg849 mutant flies.

      Expression of Hsap\L1CAMR184Q.Scer\UAS does not suppress the giant fibre axon guidance defects seen in Nrg849 mutant flies.

      Expression of Hsap\L1CAM4A.Scer\UAS does not suppress the giant fibre axon guidance defects seen in Nrg849 mutant flies.

      Expression of Hsap\L1CAMH1.Scer\UAS partially suppresses the giant fibre axon guidance defects seen in Nrg849 mutant flies.

      (Kudumala et al., 2013)

      Expression of Hsap\L1CAMScer\UAS.cGa pre- and post-synaptically, under the control of Scer\GAL4A307 in a Nrg849 heterozygous background suppresses the Nrg849 giant synapse physiological phenotype to approximately 98% of the wild-type level.

      Expression of two copies of Hsap\NCAM1Scer\UAS.cGa pre- and post-synaptically, under the control of Scer\GAL4A307 in a Nrg849 heterozygous background fails to suppresses the Nrg849 giant synapse physiological phenotype.

      Expression of two copies of Rnor\NrcamScer\UAS.cGa pre- and post-synaptically, under the control of Scer\GAL4A307 in a Nrg849 heterozygous background fails to suppresses the Nrg849 giant synapse physiological phenotype.

      Expression of two copies of Ggal\NFASCScer\UAS.cGa pre- and post-synaptically, under the control of Scer\GAL4A307 in a Nrg849 heterozygous background fails to suppresses the Nrg849 giant synapse physiological phenotype.

      Expression of Hsap\L1CAMH210Q.Scer\UAS pre- and post-synaptically, under the control of Scer\GAL4A307 in a Nrg849 heterozygous background does not suppress the Nrg849 giant synapse physiological phenotype.

      (Godenschwege et al., 2006)
      Complementation and Rescue Data
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer

      Heisenberg.

      Comments
      Comments

      Females display increased ovulation and low receptivity after Acp70A injection.

      (Fleischmann et al., 1995)

      Strains differ from wild type in one or more larval behavioural assays.

      (Varnam and Sokolowski, 1995)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (6)
      References (18)