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General Information
Symbol
Dmel\mtsXE-2258
Species
D. melanogaster
Name
FlyBase ID
FBal0048909
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
mtsXE2258
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

A 16 bp deletion that spans the translation start site.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

16bp deletion, bases -7 to 9, that spans the translation start site. The next in-frame methionine does not occur for another 66 amino acids.

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
Detailed Description
Statement
Reference

mtsXE-2258/+ mutants do not display any apparent phenotype in the thorax or wings of adult flies, nor any significant difference in survival rate, as compared to controls.

mts02496/mtsXE-2258 mutant embryos do not exhibit any defects in neuroblast division at stage 10 of embryogenesis.

mts02496/mtsXE-2258 mitotic neuroblasts display normal mira localisation.

Homozygous clones are not recovered in the eye. Germ line clones reveal that oogenesis is blocked at stage 5.

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

mtsXE-2258/mts[+] is a suppressor | partially of visible phenotype of Scer\GAL4ap-md544, Tap42GD8900

mtsXE-2258/mts[+] is a suppressor | partially of visible | dominant phenotype of hhMrt

mtsXE-2258/mts[+] is a suppressor of abnormal neurophysiology | semidominant phenotype of inaC2

mtsXE-2258 is a suppressor of visible phenotype of Dsor1XS520

NOT Suppressor of
Statement
Reference

mtsXE-2258/mts[+] is a non-suppressor of abnormal neurophysiology phenotype of norpA35

mtsXE-2258/mts[+] is a non-suppressor of abnormal neurophysiology | semidominant phenotype of inaC2

mtsXE-2258/mts[+] is a non-suppressor of abnormal neurophysiology | recessive phenotype of inaC2

Other
Phenotype Manifest In
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

mtsXE-2258/mts[+] is a suppressor | partially of wing phenotype of hhMrt

mtsXE-2258 is a suppressor of eye phenotype of Raf12

mtsXE-2258 is a suppressor of eye phenotype of Dsor1XS520

mtsXE-2258 is a suppressor of eye phenotype of Raf::tor13D.hs.sev

Additional Comments
Genetic Interactions
Statement
Reference

mtsXE-2258/+ partially rescues the cleft thorax and wing phenotypes, and rescues survival of flies expressing Tap42GD8900 under the control of Scer\GAL4ap-md544.

Compared with wild-type controls, a lower than expected proportion of the embryos hatch resulting from the cross between polo11/+, mtsXE-2258/+ mothers and wild-type fathers.

The embryos from mothers heterozygous polo11 and mtsXE-2258, of which a minority are able to hatch into larvae, show a high frequency of detached centrosomes at any stage of the mitotic cycles.

The embryos resulting from the cross between gwlscant/+, mtsXE-2258/+ mothers and wild-type fathers fail to hatch.

gwl6a/+ partially rescues the viability of embryos from mtsXE-2258/+, polo11/+ mothers.

gwlSr18/+ partially rescues the viability of embryos from mtsXE-2258/+, polo11/+ mothers.

The addition of one copy of mtsXE-2258 to l(2)gl4/l(2)glts3 flies reduces the eclosion rate to 72% and 42% respectively.

The presence of one copy of mtsXE-2258 in l(2)gl4/l(2)glts3 flies increases the frequency of defective bristle formation to 33% and 64% respectively (compared to 28% in l(2)gl4/l(2)glts3 mutants).

The deactivation defect seen in inaC2 heterozygotes is rescued in a mtsXE-2258 heterozygous background. Contrarily, heterozygosity of mtsXE-2258 fails to rescue the inactivation defect of inaC2 homozygotes. inaC2 heterozygotes and homozygotes display a deficiency in light adaptation, which fails to be rescued in both genotypes when in combination with mtsXE-2258/+.

The homozygous norpA35 deactivation defects are not rescued when in combination with mtsXE-2258/+.

Enhances the rough eye phenotype of Ras85DV12.sev. Has little or no effect on the phenotype of Ras85DN17.sev. Enhances the phenotype of phl::tor13D.hs.sev. Enhances the phenotype of Ras85D::Src64BV12.ΔCAAX.sev. Has little or no effect on the lethality of phl12. Suppresses the phl12 eye phenotype. Suppresses the Dsor1XS520 eye phenotype.

Weak enhancer of rough eye phenotype of Ras85DV12.sev. Weakly suppresses the rough eye phenotype of phl::tor13D.hs.sev. Dominantly enhances the phenotype of phl12.

Xenogenetic Interactions
Statement
Reference

The neuronal degeneration phenotype and decreased survival of animals expressing Hsap\HDQ93.ex1p.Scer\UAS under the control of Scer\GAL4elav-C155 is modestly suppressed in a mtsXE-2258/+ mutant background, but the effect is not statistically significant.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (25)