Allele Dmel\EG28EG28
| General Information | |||
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| Symbol | Dmel\EG28EG28 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0244438 | |
| Feature type | allele | Associated gene | Dmel\EG28 |
| Allele class | |||
| Mutagen | ethyl methanesulfonate | ||
Recent Updates
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References | |||
| Associated Sequence Data | |||
| DDBJ
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
| UniProtKB/TrEMBL | |||
| Progenitor genotype | |||
| Nature of the lesion | Statement Reference | ||
| Cytology | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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Detailed Description
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Statement Reference | |||
External Data
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| Linkouts | |||
Interactions
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Phenotypic Class
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Enhancer of | |||
Statement Reference EG28EG28/EG28[+] is an enhancer of neurophysiology defective | dominant | adult stage phenotype of Gl1 EG28EG28/EG28[+] is an enhancer of visible phenotype of GlΔ.Scer\UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF | |||
NOT Enhancer of | |||
Statement Reference EG28EG28/EG28[+] is a non-enhancer of neuroanatomy defective | adult stage phenotype of GlΔ.Scer\UAS, Scer\GAL4A307 | |||
Other | |||
Statement Reference | |||
Phenotype Manifest In
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Enhancer of | |||
Statement Reference | |||
NOT Enhancer of | |||
Statement Reference | |||
Other | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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Statement Reference EG28[EG28] dominantly enhances the eye phenotype caused by expression of Gl[Δ.Scer\UAS] under the control of Scer\GAL4[GMR.PF].
20% of giant fiber axons fail to exit the brain in adults expressing Gl[Δ.Scer\UAS] under the control of Scer\GAL4[A307] in a EG28[EG28]/+ background.
Only 3% of giant fiber axons in Gl[1]/+ ; EG28[EG28]/+ double heterozygotes lack the characteristic terminal bend, but the axons often show ectopic branching.
The electrophysiological defects seen in the giant fiber system of Gl[1]/+ adults are enhanced if they are also heterozygous for EG28[EG28]; the response latencies are significantly increased and the double heterozygous flies show poor following. | |||
Xenogenetic Interactions
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Statement Reference | |||
Complementation & Rescue Data
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| Comments | |||
Stocks
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Notes on Origin
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| Discoverer | |||
It has not been determined whether the lethality of the chromosome is caused by the mutation that modifies the eye phenotype caused by expression of Gl[Δ.Scer\UAS] under the control of Scer\GAL4[GMR.PF], so it is possible that the recessive lethality of the chromosome is due to a second-site mutation. | |||
External Crossreferences & Linkouts
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Synonyms & Secondary IDs
( 1 ) | |||
| Reported As | |||
| Symbol Synonym | EG28EG28 | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 1 ) | |||
| Research paper |
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Recent Updates
External Crossreferences & Linkouts