Allele Dmel\SoxN^GA1192

General Information
Symbol	Dmel\SoxN^GA1192	Species	D. melanogaster
Name		FlyBase ID	FBal0141379
Feature type	allele	Created / Updated	2006-08-22/2006-08-22
Associated gene	Dmel\SoxN

Allele class	amorph
Mutagen	ethyl methanesulfonate
Nature of the Allele
Allele class	amorph (Buescher et al., 2002)
Mutagen	ethyl methanesulfonate (Buescher et al., 2002)
Mapped Features and Mutations
Type Symbol & Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference
Assay mode
Cytology
Phenotypic Data
Phenotypic Class
	neuroanatomy defective (Buescher et al., 2002) neuroanatomy defective \| embryonic stage (Girard et al., 2006)
Phenotype Manifest In
	embryonic head (Buescher et al., 2002) midgut constriction (Buescher et al., 2002) denticle belt (Buescher et al., 2002, Chao et al., 2007) RP2 neuron (Buescher et al., 2002) EL neuron (Buescher et al., 2002) aCC neuron (Buescher et al., 2002) pCC neuron (Buescher et al., 2002) ganglion mother cell (Buescher et al., 2002) stage 1 neuroblast (Buescher et al., 2002) neuroblast NB3-5 (Buescher et al., 2002) neuroblast NB2-5 (Buescher et al., 2002) neuroblast NB5-3 (Buescher et al., 2002) neuroblast NB3-2 (Buescher et al., 2002) neuroblast NB5-6 (Buescher et al., 2002) neuroblast NB7-4 (Buescher et al., 2002) neuroblast NB2-2 (Buescher et al., 2002) neuroblast NB4-2 (Buescher et al., 2002) neuroblast NB6-2 (Buescher et al., 2002) neuroblast NB7-2 (Buescher et al., 2002) neuroblast NB3-1 (Buescher et al., 2002) neuroblast NB4-1 (Buescher et al., 2002) neuroblast NB6-1 (Buescher et al., 2002) neuroblast NB6-4 (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) neuroblast NB2-1 (Buescher et al., 2002) neuroblast NB2-4 (Buescher et al., 2002) neuroblast NB3-3 (Buescher et al., 2002) neuroblast NB4-4 (Buescher et al., 2002) neuroblast NB5-4 (Buescher et al., 2002) neuroblast NB5-1 (Buescher et al., 2002) neuroblast NB4-3 (Buescher et al., 2002) neuroblast NB5-5 (Buescher et al., 2002) neuroblast NB7-3 (Buescher et al., 2002) neuroblast NB1-1 (Buescher et al., 2002) neuroblast MP2 (Buescher et al., 2002) neuroblast NB5-2 (Buescher et al., 2002) embryonic/first instar larval cuticle (Chao et al., 2007) axon & ventral nerve cord (Girard et al., 2006) anterior commissure (Girard et al., 2006) posterior commissure (Girard et al., 2006)
Detailed Description
	Statement Reference 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 SoxN^GA1192 double mutant embryos show a combination of the neurogenic E(spl)^rv1 phenotype and the anti-neural SoxN^GA1192 phenotype. The neurogenic phenotype is apparent in the ventral column of the S1 neuroblasts. In the lateral column, the anti-neural phenotype of SoxN^GA1192 remains unchanged in the double mutant embryos. (Buescher et al., 2002) SoxN[GA1192] 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)
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Other
Statement Reference SoxN^GA1192, lola[+]/lola⁰⁰⁶⁴² has lethal \| partially phenotype (Girard et al., 2006) SoxN^GA1192, beat-Ia[+]/beat-Ia³ has semi-lethal phenotype (Girard et al., 2006) SoxN^GA1192, Ubx[+]/Ubx¹⁰¹ has lethal phenotype (Girard et al., 2006) SoxN^GA1192, tup¹/tup[+] has lethal \| partially phenotype (Girard et al., 2006)
Phenotype Manifest In
Enhanced by
Statement Reference SoxN^GA1192 has neuroblast NB5-3 phenotype, enhanceable by D⁸⁷ (Buescher et al., 2002) SoxN^GA1192 has neuroblast NB1-1 phenotype, enhanceable by D⁸⁷ (Buescher et al., 2002) SoxN^GA1192 has embryonic/first instar larval cuticle phenotype, enhanceable by pan[+]/pan² (Chao et al., 2007) SoxN^GA1192 has denticle belt phenotype, enhanceable by pan[+]/pan² (Chao et al., 2007)
NOT Enhanced by
Statement Reference SoxN^GA1192 has stage 1 neuroblast phenotype, non-enhanceable by Dr^ltt-EMS (Buescher et al., 2002)
Enhancer of
Statement Reference SoxN^GA1192 is an enhancer of neuroblast NB5-3 phenotype of D⁸⁷ (Buescher et al., 2002) SoxN^GA1192 is an enhancer of neuroblast NB1-1 phenotype of D⁸⁷ (Buescher et al., 2002)
Other
Statement Reference SoxN^GA1192, lola[+]/lola⁰⁰⁶⁴² has longitudinal connective phenotype (Girard et al., 2006) SoxN^GA1192, lola[+]/lola⁰⁰⁶⁴² has anterior commissure phenotype (Girard et al., 2006) SoxN^GA1192, lola[+]/lola⁰⁰⁶⁴² has posterior commissure phenotype (Girard et al., 2006) SoxN^GA1192, lola[+]/lola⁰⁰⁶⁴² has axon phenotype (Girard et al., 2006) SoxN^GA1192, beat-Ia[+]/beat-Ia³ has anterior commissure phenotype (Girard et al., 2006) SoxN^GA1192, beat-Ia[+]/beat-Ia³ has posterior commissure phenotype (Girard et al., 2006) SoxN^GA1192, beat-Ia[+]/beat-Ia³ has longitudinal connective phenotype (Girard et al., 2006)
Additional Comments
Genetic Interactions
Statement Reference The NB1-1 neuroblast fails to form in 48% of hemisegments in D⁸⁷ SoxN^GA1192 double mutant embryos. The NB5-3 neuroblast fails to form in 25% of hemisegments in D⁸⁷ SoxN^GA1192 double mutant embryos. (Buescher et al., 2002) Approximately 58.2% of arm[4]/+ ; SoxN[GA1192]/+ double mutants appear phenotypically wild-type. Approximately 17.4% of mutants exhibit a 'lawn of denticles' phenotype, typical of arm mutants. The SoxN[GA1192] 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 pan[2]/+ ; SoxN[GA1192]/+ double mutants appear phenotypically wild-type. Approximately 19.2% of mutants exhibit a 'lawn of denticles' phenotype, typical of arm mutants. The SoxN[GA1192] 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 SoxN[GA1192] single mutants. (Chao et al., 2007) Sema-2a[03021]/+; SoxN[GA1192]/+ mutants are viable. lola[00642]/+, SoxN[GA1192]/+ 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/+, SoxN[GA1192]/+ 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 SoxN[GA1192]/+ embryos. (Girard et al., 2006)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	SoxN^GA1192 (Chao et al., 2007, Girard et al., 2006)
Name Synonym
Secondary FlyBase IDs

References ( 3 )
Research paper	Chao et al., 2007, Development 134(5): 989--997 The HMG-box transcription factor SoxNeuro acts with Tcf to control Wg/Wnt signaling activity. [FBrf0195251] Girard et al., 2006, Dev. Biol. 299(2): 530--542 Chromatin immunoprecipitation reveals a novel role for the Drosophila SoxNeuro transcription factor in axonal patterning. [FBrf0194303] Buescher et al., 2002, Development 129(18): 4193--4203 Formation of neuroblasts in the embryonic central nervous system of Drosophila melanogaster is controlled by SoxNeuro. [FBrf0151914]

Allele Dmel\SoxNGA1192

Allele Dmel\SoxN^GA1192