Allele Dmel\inv30
| General Information | |||
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| Symbol | Dmel\inv30 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0045908 | |
| Feature type | allele | Associated gene | Dmel\inv |
| Allele class | loss of function allele, amorphic allele - genetic evidence | ||
| Mutagen | Delta2-3 | ||
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 Small deficiency removing the first exon. Intragenic deletion removing most of the inv transcription unit. The portion of the gene encoding the homeodomain is left intact. Intragenic deletion removing approximately 27kb of the inv transcription unit, including the transcription start site, the first two exons and most of the second intron. | ||
| 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 Gaps are seen in the posterior of the hindgut boundary cell rows in mutant embryos. The development of the border cells of the hindgut (which normally form an anterior and posterior ring at the ends of the hindgut and bilateral strands that connect the two rings) is not affected in mutant embryos. Homozygous embryos do not show duplications of the RP2 neuron. Survives without abnormality over Df(2R)en-SFX31, except for slight defects on the anterior crossvein. Adult flies are normal in appearance. | |||
External Data
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Interactions
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Phenotypic Class
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Other | |||
Statement Reference | |||
Phenotype Manifest In
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Other | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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Statement Reference Approximately 34% of fra[1]/inv[30] double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Approximately 87% of the segments are affected in these embryos.
Approximately 15% of fra[1]/inv[30] double mutants are adult lethal. | |||
Xenogenetic Interactions
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Statement Reference | |||
Complementation & Rescue Data
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| Comments | |||
Stocks
( 1 ) | |||
| Bloomington | 7088 | ||
Notes on Origin
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| Discoverer | |||
External Crossreferences & Linkouts
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| Other Crossreferences | |||
| Linkouts | |||
Synonyms & Secondary IDs
( 2 ) | |||
| Reported As | |||
| Symbol Synonym | Df(2R)inv30 inv30 | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 6 ) | |||
| Research paper |
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Recent Updates
External Crossreferences & Linkouts