Allele Dmel\vn10567
| General Information | |||
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| Symbol | Dmel\vn10567 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0009626 | |
| Feature type | allele | Associated gene | Dmel\vn |
| Also Known As | vnP1749 | ||
| Map ( GBrowse ) |
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| Allele class | loss of function allele | ||
| Mutagen | P-element activity | ||
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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 transposable element insertion site | |||
| 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 P{PZ} insertion within the first non-coding exon. | ||
| Caused by insertion | |||
| 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 Whereas wild-type adult midgut progenitor cells (AMPs) form many large clusters, few AMP clusters are found in late larval vn[10567] and vn[10567]/vn[γ7] mutant midguts.
Most vn[10567]/vn[γ7] mutants die as pharate adults.
Lineage analysis of marked clones reveals that vn[10567]/vn[γ7] mutants display a failure of proliferation of AMPs during early larval stages, although the number of AMPs generated initially during embryogenesis is not different between mutants and wild-type controls. The size of the few remaining AMP clusters in vn[10567]/vn[γ7] mutants is relatively normal, suggesting that the late phase of AMP proliferation is largely unaffected in these mutants.
Expression of vn[Scer\UAS.cSa] in larval enterocytes driven by Scer\GAL4[Myo31DF-NP0001] not only rescues the adult midgut progenitor cell phenotype of vn[10567] mutants, but it also causes ectopic AMP cell proliferation. Late stage vn10567/Df(3L)v65c embryos lack lch5 ligament attachment cells. Border cells still migrate dorsally when all dorsal follicle cells are mutant for vn10567 in females containing homozygous clones. A significant number of somatic muscle fibres show multiple, mis-guided membrane extensions at their leading edges. The DA1 muscle precursor is sometimes missing. Abnormal muscle phenotype. Myotubes of mutant embryos are elongated and continuously send filopodia in random directions. | |||
External Data
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| Linkouts | |||
Interactions
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Phenotypic Class
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Enhancer of | |||
Statement Reference | |||
Suppressor of | |||
Statement Reference | |||
Other | |||
Statement Reference | |||
Phenotype Manifest In
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Enhanced by | |||
Statement Reference vn10567 has abdominal 2 dorsal acute muscle 1 | precursor phenotype, enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B/EgfrDN.Scer\UAS vn10567 has abdominal 3 dorsal acute muscle 1 | precursor phenotype, enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B/EgfrDN.Scer\UAS vn10567 has abdominal 4 dorsal acute muscle 1 | precursor phenotype, enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B/EgfrDN.Scer\UAS vn10567 has abdominal 5 dorsal acute muscle 1 | precursor phenotype, enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B/EgfrDN.Scer\UAS vn10567 has abdominal 6 dorsal acute muscle 1 | precursor phenotype, enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B/EgfrDN.Scer\UAS vn10567 has abdominal 7 dorsal acute muscle 1 | precursor phenotype, enhanceable by Scer\GAL4how-24B/Scer\GAL4how-24B/EgfrDN.Scer\UAS | |||
Enhancer of | |||
Statement Reference vn[+]/vn10567 is an enhancer of ommatidium phenotype of Scer\GAL4ey.PH, brmK804R.Scer\UAS.T:Ivir\HA1 | |||
Suppressor of | |||
Statement Reference vn[+]/vn10567 is a suppressor of wing vein | ectopic phenotype of Scer\GAL4tub.PU, cswN308D.Scer\UAS.P\T | |||
Other | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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Statement Reference 2/3 of vn10567; rhounspecified double homozygous embryo cuticles show a general loss of cuticle integrity. Of the remaining 1/3 of cuticles the percentage with >2 denticle belt fusions is increased from <10% for rhounspecified to >30%. (Note, while the authors do not name an rho allele for this analysis, they do claim to have used a null allele.) The loss of the DA1 muscle precursor in vn10567 embryos is enhanced if they are also carrying EgfrDN.Scer\UAS expressed under the control of Scer\GAL4how-24B. The loss of the DA1 muscle precursor seen in vn10567 embryos is dominantly enhanced by spi3. | |||
Xenogenetic Interactions
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Statement Reference | |||
Complementation & Rescue Data
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| Fails to complement | |||
| Rescued by | |||
| Comments | Expression of vn[Scer\UAS.cSa] in larval enterocytes driven by Scer\GAL4[Myo31DF-NP0001] not only rescues the adult midgut progenitor cell phenotype of vn[10567] mutants, but it also causes ectopic AMP cell proliferation.
Expression of vn[Scer\UAS.cSa] in adult midgut progenitor cells (AMPs) rescues the AMP cell proliferation phenotype of vn[10567] mutants.
Expression of vn[Scer\UAS.cSa] in visceral muscle driven by Scer\GAL4[how-24B] rescues the adult midgut progenitor cell phenotype of vn[10567] mutants. | ||
Stocks
( 1 ) | |||
| Bloomington | |||
Notes on Origin
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| Discoverer | A. Spradling. | ||
Comments
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Precise excision of the P{PZ} insertion completely reverses the muscle phenotype and results in full viability. Results indicate the insertion is responsible for the phenotype. Complements: Bre101640. Complements: l(3)0233102331. Complements: l(3)0514305143. Complements: l(3)neo111. | |||
External Crossreferences & Linkouts
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| Other Crossreferences | |||
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Synonyms & Secondary IDs
( 6 ) | |||
| Reported As | |||
| Symbol Synonym | l(3)10567 l(3)1056710567 l(3)vn10567 P1749 vn10567 | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 18 ) | |||
| Research paper |
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| Personal communication to FlyBase |
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Recent Updates
External Crossreferences & Linkouts