FB2024_03 , released June 25, 2024
Allele: Dmel\SoxNGA1192
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General Information
Symbol
Dmel\SoxNGA1192
Species
D. melanogaster
Name
FlyBase ID
FBal0141379
Feature type
allele
Associated gene
Dmel\SoxN
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Buescher et al., 2002)
Mutagen
ethyl methanesulfonate
(Buescher et al., 2002)
Progenitor genotype
Cytology
Description

Nucleotide substitution: C?T.

(Overton et al., 2007)

Amino acid replacement: ?172term.

(Overton et al., 2007)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2L:8,827,010..8,827,010 [+]
Nucleotide change:

C8827010T

Reported nucleotide change:

C?T

Amino acid change:

Q173term | SoxN-PA; Q173term | SoxN-PB

Reported amino acid change:

?172term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change. Curator note: annotated amino acid position of mutation off by one from reported position but fits the reported nucleotide change.

(Overton et al., 2002)
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
      Phenotype Manifest In

      axon & ventral nerve cord

      (Girard et al., 2006)

      denticle

      (Overton et al., 2007)

      embryonic/first instar larval cuticle

      (Chao et al., 2007, Overton et al., 2007)

      embryonic head

      (Buescher et al., 2002)

      embryonic midgut constriction

      (Buescher et al., 2002)

      ganglion mother cell

      (Buescher et al., 2002)

      larval anterior commissure

      (Girard et al., 2006)

      larval DA1 motor neuron

      (Buescher et al., 2002)

      larval EL neuron

      (Buescher et al., 2002)

      larval posterior commissure

      (Girard et al., 2006)

      larval RP2 motor neuron

      (Buescher et al., 2002)

      neuroblast MP2

      (Buescher et al., 2002)

      neuroblast NB1-1

      (Buescher et al., 2002)

      neuroblast NB2-1

      (Buescher et al., 2002)

      neuroblast NB2-2

      (Buescher et al., 2002)

      neuroblast NB2-4

      (Buescher et al., 2002)

      neuroblast NB2-5

      (Buescher et al., 2002)

      neuroblast NB3-1

      (Buescher et al., 2002)

      neuroblast NB3-2

      (Buescher et al., 2002)

      neuroblast NB3-3

      (Buescher et al., 2002)

      neuroblast NB3-5

      (Buescher et al., 2002)

      neuroblast NB4-1

      (Buescher et al., 2002)

      neuroblast NB4-2

      (Buescher et al., 2002)

      neuroblast NB4-3

      (Buescher et al., 2002)

      neuroblast NB4-4

      (Buescher et al., 2002)

      neuroblast NB5-1

      (Buescher et al., 2002)

      neuroblast NB5-2

      (Buescher et al., 2002)

      neuroblast NB5-3

      (Buescher et al., 2002)

      neuroblast NB5-4

      (Buescher et al., 2002)

      neuroblast NB5-5

      (Buescher et al., 2002)

      neuroblast NB5-6

      (Buescher et al., 2002)

      neuroblast NB6-1

      (Buescher et al., 2002)

      neuroblast NB6-2

      (Buescher et al., 2002)

      neuroblast NB6-4

      (Buescher et al., 2002)

      neuroblast NB7-2

      (Buescher et al., 2002)

      neuroblast NB7-3

      (Buescher et al., 2002)

      neuroblast NB7-4

      (Buescher et al., 2002)

      pCC neuron

      (Buescher et al., 2002)

      stage 1 neuroblast

      (Buescher et al., 2002)

      stage 2 neuroblast

      (Buescher et al., 2002)

      stage 3 neuroblast

      (Buescher et al., 2002)

      stage 4 neuroblast

      (Buescher et al., 2002)

      stage 5 neuroblast

      (Buescher et al., 2002)

      ventral denticle belt

      (Chao et al., 2007, Buescher et al., 2002)
      Detailed Description
      Statement
      Reference

      Homozygous embryos show a moderate loss of denticles and a corresponding increase in naked cuticle.

      (Overton et al., 2007)

      SoxNGA1192 embryos show defects in the axon scaffolding in the ventral nerve cord, including disruption of the longitudinal axon fascicles, and strong defects in the anterior and posterior commissures.

      (Girard et al., 2006)

      Mutant embryos show a severe loss of anterior setae which results in a reduction of the anterio-posterior expansion of the denticle belts. There are defects in head formation and in gut constrictions. Mutant embryos show a drastic loss of neurons; for eve-positive neurons there is a 98% loss of RP2 neurons and a 100% loss of EL neuron clusters. The aCC/pCC neurons are only slightly affected (3% loss), and CQ neurons are unaffected. There is also a loss of the parental eve-expressing ganglion mother cells (GMCs), with the frequency of their loss being comparable to that of the loss of their respective neuronal progeny. There is also a severe loss of ftz-positive GMCs and neurons, with the loss occurring mostly in the intermediate and lateral regions of the central nervous system (the ventralmost region forms almost normally). Mutant embryos show loss of neuroblasts (NBs) from the lateral and intermediate regions of the neuroectoderm, while the ventral region is much less affected. Late arising NBs are more severely affected than early arising NBs. NBs that arise at the same time and in the same column are differentially affected. Formation of S1 neuroblasts in the lateral and intermediate columns is severely impaired in stage 9 mutant embryos. Only 1 or 2 NBs are formed in the lateral column per hemisegment (compared to 4 in wild type). Different lateral NBs are differentially affected; NB2-5 fails to form in 22% of hemisegments, NB5-6 fails to form in 82%, NB3-5 fails to form in 60% and NB7-4 fails to form in 66%. In the intermediate column, NB5-3 fails to form in 14% of hemisegments, while NB3-2 fails to form in 67% of hemisegments. The four NBs of the ventral column form almost normally (3% loss for NB1-1, 1% loss for MP2, 2% loss for NB5-2 and 0% loss for NB7-1). Loss of S2 neuroblasts is seen in mutant embryos. In the ventral region of the neuroectoderm, NB2-2 shows 8% loss, and in the intermediate region, NB4-2 shows 98% loss, NB6-2 shows 65% loss and NB7-2 shows 86% loss. Loss of S3 neuroblasts is seen in mutant embryos. In the ventral region of the neuroectoderm, NB3-1 shows 10% loss, NB4-1 shows 7% loss and NB6-1 shows 12% loss, and in the lateral region, NB6-4 shows 97% loss and aGB shows 0% loss. Loss of S4 neuroblasts is seen in mutant embryos. In the ventral region of the neuroectoderm, NB2-1 shows 9% loss, and in the lateral region, NB2-4 shows 98% loss, NB3-3 shows 100% loss, NB4-4 shows 99% loss and NB5-4 shows 24% loss. Loss of S5 neuroblasts is seen in mutant embryos. In the ventral region of the neuroectoderm, NB5-1 shows 6% loss, and in the lateral region, NB4-3 shows 100% loss, NB5-5 shows 95% loss and NB7-3 shows 100% loss. E(spl)rv1 SoxNGA1192 double mutant embryos show a combination of the neurogenic E(spl)rv1 phenotype and the anti-neural SoxNGA1192 phenotype. The neurogenic phenotype is apparent in the ventral column of the S1 neuroblasts. In the lateral column, the anti-neural phenotype of SoxNGA1192 remains unchanged in the double mutant embryos.

      (Buescher et al., 2002)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Enhanced by
      Statement
      Reference

      SoxNGA1192 has embryonic/first instar larval cuticle phenotype, enhanceable by pan[+]/pan2

      (Chao et al., 2007)

      SoxNGA1192 has ventral denticle belt phenotype, enhanceable by pan[+]/pan2

      (Chao et al., 2007)

      SoxNGA1192 has neuroblast NB5-3 phenotype, enhanceable by D87

      (Buescher et al., 2002)

      SoxNGA1192 has neuroblast NB1-1 phenotype, enhanceable by D87

      (Buescher et al., 2002)
      NOT Enhanced by
      Statement
      Reference

      SoxNGA1192 has stage 1 neuroblast phenotype, non-enhanceable by Drltt-EMS

      (Buescher et al., 2002)
      Enhancer of
      Statement
      Reference

      SoxNGA1192 is an enhancer of neuroblast NB5-3 phenotype of D87

      (Buescher et al., 2002)

      SoxNGA1192 is an enhancer of neuroblast NB1-1 phenotype of D87

      (Buescher et al., 2002)
      Suppressor of
      Statement
      Reference

      SoxNGA1192 is a suppressor of denticle | ectopic phenotype of EgfrAct.cUa.UAS, Scer\GAL4sca.PU

      (Overton et al., 2007)
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Approximately 58.2% of arm4/+ ; SoxNGA1192/+ double mutants appear phenotypically wild-type. Approximately 17.4% of mutants exhibit a 'lawn of denticles' phenotype, typical of arm mutants. The SoxNGA1192 mutation disrupts the dorsal pattern and reduces the size of the embryos. A SoxN-like phenotype is observed in approximately 17.6% of the double mutants. Approximately 6.8% of the double mutants exhibit a severe arm phenotype.

      Approximately 55.9% of pan2/+ ; SoxNGA1192/+ double mutants appear phenotypically wild-type. Approximately 19.2% of mutants exhibit a 'lawn of denticles' phenotype, typical of arm mutants. The SoxNGA1192 mutation disrupts the dorsal pattern and reduces the size of the embryos. A SoxN-like phenotype is observed in approximately 17.7% of the double mutants. Approximately 7.2% of the double mutants exhibit a severe excess-naked-cuticle SoxN-like phenotype. The double mutants exhibit more extensive naked cuticle than SoxNGA1192 single mutants.

      (Chao et al., 2007)

      The ectopic denticle formation seen in larvae expressing EgfrAct.cUa.Scer\UAS under the control of Scer\GAL4sca.PU is strongly reduced by SoxNGA1192.

      (Overton et al., 2007)

      Sema-2a03021/+; SoxNGA1192/+ mutants are viable.

      lola00642/+, SoxNGA1192/+ double heterozygous embryos show defects in axon scaffolding, such as fusion of commissures, axonal tangles, disruption and/or reduction of longitudinal connectives. This phenotype is not seen in either single mutant heterozygote.

      beat-Ia/+, SoxNGA1192/+ double heterozygous embryos commissures are partially fused and the longitudinal connectives are thinner or missing. This phenotype is not seen in either beat-Ia/+ or SoxNGA1192/+ embryos.

      (Girard et al., 2006)

      The NB1-1 neuroblast fails to form in 48% of hemisegments in D87 SoxNGA1192 double mutant embryos. The NB5-3 neuroblast fails to form in 25% of hemisegments in D87 SoxNGA1192 double mutant embryos.

      (Buescher et al., 2002)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (1)
      Reported As
      Symbol Synonym
      SoxNGA1192
      (Stagg et al., 2011, Chao et al., 2007, Overton et al., 2007, Girard et al., 2006)
      Name Synonyms
      Secondary FlyBase IDs
        References (5)