FB2024_03 , released June 25, 2024
Allele: Dmel\eveUAS.cBa
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General Information
Symbol
Dmel\eveUAS.cBa
Species
D. melanogaster
Name
Saccharomyces cerevisiae UAS construct a of Brand
FlyBase ID
FBal0031220
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-eve
Key Links
Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

UASt regulatory sequences drive expression of a cDNA-genomic DNA fusion encoding eve.

Allele components
Component
Use(s)
Encoded product / tool
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

abdominal 3 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 3 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 3 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 3 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 3 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 3 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 3 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 3 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 3 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 3 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 4 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 4 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 4 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 4 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 4 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 4 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 4 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 4 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 4 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 4 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 5 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 5 lateral transverse muscle 1 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 5 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 5 lateral transverse muscle 2 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 5 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 5 lateral transverse muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 5 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 5 lateral transverse muscle 4 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal 5 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4elav-C155

abdominal 5 ventral longitudinal muscle 3 & neuromuscular junction, with Scer\GAL4ftz.ng

abdominal posterior fascicle & abdominal segment 3, with Scer\GAL4elav-C155

abdominal posterior fascicle & abdominal segment 3, with Scer\GAL4ftz.ng

abdominal posterior fascicle & abdominal segment 4, with Scer\GAL4elav-C155

abdominal posterior fascicle & abdominal segment 4, with Scer\GAL4ftz.ng

abdominal posterior fascicle & abdominal segment 5, with Scer\GAL4elav-C155

abdominal posterior fascicle & abdominal segment 5, with Scer\GAL4ftz.ng

Detailed Description
Statement
Reference

Misexpression of eveScer\UAS.cBa in EW neurons, under the control of Scer\GAL4eg-Mz360 transcriptionally reprograms EW interneurons to express the same array of molecules as in dorsal interneurons. These EW neurons no longer cross the CNS midline and remain ipsilateral, with some projecting towards the muscle field.

In almost all EW neurons, misexpressing eveScer\UAS.cBa axons fail to cross the midline and in 25% of hemisegments project laterally and join the motor roots.

The number of nuclei resulting from the ectopic expression of eveScer\UAS.cBa in DT1 and VA2 muscles under the control of Scer\GAL4kirre.PR increases from the wild-type number of 8 for DT1 and 9 for VA2 to numbers that are more characteristic of DA1.

Expression of eveScer\UAS.cBa in dMP2 neurons, under the control of Scer\GAL4Vap.P0201 can trigger lateral ventral nerve cord exit of dMP2 at low frequency (approximately 5.5%).

Misexpression of eveScer\UAS.cBa, under the control of Scer\GAL4elav.PLu, results in aberrant dorsal projection of both ventral-ISNb and lateral-SNa branches, leading to the joining of these branches with the dorsal branch of the ISN.

Anterior-posterior polarization of cells in the extending germband is disrupted in eveScer\UAS.cBa; Scer\GAL4mat.αTub67C.T:Hsim\VP16 embryos. This disruption correlates with a failure of germband extension. (Note: The embryos analysed in these experiments were mosaics - due to the presence of ldsHor-1, which induces the sporadic loss of paternally derived chromosomes).

In eveScer\UAS.cBa; Scer\GAL4how-24B embryos, the cardiac outflow muscles do not attach to the tip of the heart, but instead extend anteriorly and attach to invaginating heart-anchoring cells (HANC), which are no longer able to anchor properly the tip of the heart. The main cardiac outflow muscle branch that normally attaches to the cardiac outflow region is absent or fused with the HANC-attaching branch. The same phenotypes are seen in eveScer\UAS.cBa; Scer\GAL4tin.cBa embryos, albeit with lower penetrance.

When eveScer\UAS.cBa is driven by Scer\GAL4how-24B, a significant number if cells from the dorsal mesoderm assume altered identities. Losses of heart cells and cardioblasts are seen.

eveScer\UAS.cBa when driven by Scer\GAL4cad-em459 causes an enlargement of the adult hindgut primordium.

When expression is driven by Scer\GAL4elav-C155 or Scer\GAL4ftz.ng, all peripheral nerve branches fuse. Ventral and lateral muscles left initially uninnervated eventually form neuromuscular junctions, though the position of the neuromuscular junctions on the muscles is often abnormal. The delayed-formation neuromuscular junctions show wild-type neuromuscular target recognition.

When eve is expressed in the expression pattern of h using Scer\GAL4h-1J3, the cuticles prepared from the dead embryos exhibit extra denticles between alternating segments, in regions that are normally naked.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

CNS exit from EW neurons misexpressing eveScer\UAS.cBa is partially suppressed in an unc-58 mutant background and midline crossing is partially restored.

CNS exit from EW neurons misexpressing eveScer\UAS.cBa is partially suppressed in an unc-58 beat-IaC163/beat-Ia3 mutant background while midline crossing is partially restored (in 15% of hemisegments).

Combined expression of eveScer\UAS.cBa with zfh1Scer\UAS.cZa in EW neurons, under the control of Scer\GAL4eg-Mz360, leads to a strong lateral exit of EW neurons in 80% of hemisegments.

Combined expression of eveScer\UAS.cBa with grnScer\UAS.cZa in EW neurons, under the control of Scer\GAL4eg-Mz360, leads to a strong lateral exit of EW neurons in 72% of hemisegments.

Scer\GAL4eve.eme-mediated expression of eveScer\UAS.cBa rescues the reduced number of pericardial cells in lbeeve.SS larvae.

Scer\GAL4eve.eme-mediated expression of eveScer\UAS.cBa rescues the reduced heart diameter of lbeeve.SS adults, and partially rescues the reduced diastolic and systolic diameters seen in live lbeeve.SS hearts.

Scer\GAL4eve.eme-mediated expression of eveScer\UAS.cBa rescues the myofibrillar structure defects of lbeeve.SS adult hearts.

Expression of grnScer\UAS.cBa and eveScer\UAS.cBa in dMP2 neurons, under the control of Scer\GAL4Vap.P0201 enhances the eveScer\UAS.cBa dMP2 pathfinding defect, resulting in a high frequency of lateral exit out from the ventral nerve cord (in approximately 45% of cases).

The fusion of peripheral nerve branches with the ISN seen when eveScer\UAS.cBa expression is driven by Scer\GAL4elav-C155 can be partially suppressed by simultaneous expression of beat-IaScer\UAS.cFa.

Ectopic expression of eveScer\UAS.cBa under the control of Scer\GAL4twi.PG in a zfh12 background restores the formation of some eve-expressing pericardial cells.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Phenotype dependent on Scer\GAL4.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
eveScer\UAS.cBa
eveUAS.cBa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Brand
Secondary FlyBase IDs
    References (19)