FlyBase Allele Report: Dmel\spen[AH393]

General Information

Symbol

Dmel\spen^AH393

Species

D. melanogaster

Name

FlyBase ID

FBal0103540

Feature type

allele

Associated gene

Dmel\spen

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

X ray

(Rebay et al., 2000)

ethyl methanesulfonate

(Rebay et al., 2000)

Progenitor genotype

Cytology

Description

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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 ( 1 )

Disease

Interaction

References

exacerbates autosomal dominant cerebellar ataxia

modeled by Hsap\ATXN8OS^CTG112.UAS

(Mutsuddi et al., 2004)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

lethal | recessive

(Rebay et al., 2000)

Phenotype Manifest In

central nervous system

(Chen and Rebay, 2000)

larval longitudinal connective

(Chen and Rebay, 2000)

midline glial cell

(Chen and Rebay, 2000)

symmetrical commissure

(Chen and Rebay, 2000)

Detailed Description

Statement

Reference

In mutant embryos, the midline glia cells (MGCs) are reduced in number and do not ensheathe the commissures, as seen in wild-type, leading to reduced separation between the anterior and posterior commissure bundles. At stage 12 MGCs appear normal, at stage 13 a migration defects is apparent and by stage 17 fewer (1-2 per segment) MGCs persist than seen in wild-type (about 3 per segment). Mutants also have collapsed commissures, reduced separation between the two longitudinal branches, and gaps and inappropriate crossing of the midline by the longitudinal axons producing a fragmented and disorganised longitudinal axonal array. spen^AH393/+ embryos show central nervous system defects in about 4% of embryos.

(Chen and Rebay, 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

spen^AH393 is an enhancer of abnormal neuroanatomy phenotype of Hsap\ATXN8OS^CTG112.UAS, Scer\GAL4^GMR.PF

(Mutsuddi et al., 2004)

Suppressor of

Statement

Reference

spen[+]/spen^AH393 is a suppressor of visible | dominant phenotype of N^55e11

(Kankel et al., 2007)

Other

Statement

Reference

Raf¹², spen^AH393 has lethal phenotype

(Rebay et al., 2000)

Raf¹², spen^AH393 has lethal | dominant phenotype

(Rebay et al., 2000)

Phenotype Manifest In

Enhanced by

Statement

Reference

spen^AH393 has larval longitudinal connective phenotype, enhanceable by pnt^unspecified/pnt[+]

(Chen and Rebay, 2000)

spen^AH393 has central nervous system phenotype, enhanceable by pnt^unspecified/pnt[+]

(Chen and Rebay, 2000)

Enhancer of

Statement

Reference

spen^AH393 is an enhancer of ommatidium phenotype of Hsap\ATXN8OS^CTG9.UAS, Scer\GAL4^GMR.PF

(Mutsuddi et al., 2004)

spen^AH393 is an enhancer of ommatidium phenotype of Hsap\ATXN8OS^CTG112.UAS, Scer\GAL4^GMR.PF

(Mutsuddi et al., 2004)

spen^AH393 is an enhancer of eye phenotype of Ras85D^N17.sev

(Rebay et al., 2000)

spen^AH393 is an enhancer of eye phenotype of aop^S2382

(Rebay et al., 2000)

spen^AH393 is an enhancer of eye phenotype of aop^ACT.sev

(Rebay et al., 2000)

spen^AH393 is an enhancer of eye phenotype of aop^ACT.GMR

(Rebay et al., 2000)

NOT Enhancer of

Statement

Reference

spen^AH393 is a non-enhancer of phenotype of Ras85D^V12.sev

(Rebay et al., 2000)

Suppressor of

Statement

Reference

spen[+]/spen^AH393 is a suppressor of wing phenotype of N^55e11

(Kankel et al., 2007)

NOT Suppressor of

Statement

Reference

spen^AH393 is a non-suppressor of phenotype of Ras85D^V12.sev

(Rebay et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

Dominantly suppresses the Df(1)N-54l9/+ and N^55e11/+ wing nicking phenotypes.

(Kankel et al., 2007)

when pnt^unspecified/+ is added to spen^AH393 heterozygotes, about 25% of embryos exhibit axonal defects. The predominant phenotype is reduced separation between the two longitudinal axon pathways and an occasional inappropriate crossing of the midline.

(Chen and Rebay, 2000)

Effect on aop^S2382 and Ras85D^N17.sev is mild. Effect on aop^ACT.GMR is moderate. Effect on aop^ACT.sev is strong. Lethal in combination with phl¹² at 18^oC.

(Rebay et al., 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

spen^BU720

(Rebay et al., 2000)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

"X ray" was stated as tentative. "ethyl methanesulfonate" was stated as tentative.

(Rebay et al., 2000)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

spen^AH393

(Kankel et al., 2007)

Name Synonyms

Secondary FlyBase IDs

References (4)

Report Sections

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