Open Close
General Information
Symbol
Dmel\esgG66
Species
D. melanogaster
Name
FlyBase ID
FBal0039323
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
esgG66B, esg-lacZ
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

The 3.5kb of esg sequences between esg coordinates 680 and 4200 have been deleted. A copy of the P{enG} transposon of the progenitor has flipped orientation and is now inserted at esg coordinate 4200.

Contains the P{enG} transposon in the opposite orientation from the progenitor, downstream of the esg coding region. Approximately 3kb DNA of esg coding sequence between nucleotides 800 and 4100 has been deleted.

Insertion components
P{enG}esgG66
Expression Data
Reporter Expression
distribution deduced from reporter
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Information
Statement
Reference

Expressed in a tight cluster of somatic gonadal precursor cells at the anterior of embryonic stage 17 male gonads. It is also expressed in the adult hub. It is not expressed in female gonads.

 
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

No defects in dendrite pruning of ddaC dorsal dendritic arborising neurons are seen in homozygous clones at 18 hours after puparium formation.

2o and 3o pigment cells in esgG66 clones of the eye form a cell lattice at ~36 hours APF as occurs in wild-type eyes. However, the cells in the clone fail to undergo the apical restriction that usually follows the lattice stage. Cells within the clone show no obvious defects in actin cytoskeleton or cellular morphology.

esgG66 clones in the adult eye show a dramatic loss of 2o and 3o pigment cells resulting in gaps between ommatidia.

Transplantation experiments in which prospective germ cells from homozygous esgG66 embryos are transplanted into agametic hosts show that esg is dispensible for gametogenesis in both the male and the female germline as fertile male and female host animals which have integrated homozygous esgG66 donor germ cells have been recovered.

The size of the primary branches of the tracheal system is largely unaffected in mutant embryos, even though segments of the dorsal trunk are disconnected.

Homozygous clones induced in the leg disc at the late second larval instar stage are sometimes associated with ectopic fold formation.

The dorsal branch fusion cells form discrete branches that never meet or join. These cells go on to form additional branches that resemble normal terminal branches in the larva. Lateral trunk fusion branches are completely missing leaving a gap in each segment of the lateral trunk.

Failure of tracheal fusion in embryos. Tip cells do not accumulate shg in their filopodia, which migrate in other directions and no fusion occurs. Cell motility is hyperactivated in tip cells of both thin and thick tracheal branches. esgG66 P{HS-esg.F} embryos heat shocked seven times exhibit restoration of shg expression and adhesion, the trachea completely fuse.

10-50% of homozygotes die as embryos, the rest die as larvae. esgG66/esgG66-R flies are viable.

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

esgG66, sna1 clones that express both wordsRNA.842.Scer\UAS and wordsRNA.1701.Scer\UAS, under the control of Scer\GAL4Act5C.PP, in the eye show ectopic photoreceptor and cone cells and a significant reduction of the pigment rim.

esgG66, sna1 clones show the same loss of 2o and 3o pigment cells as esgG66 clones. This phenotype is not enhanced in esgG66, sna1 Scer\GAL4Act5C.PP>wordsRNA.842.Scer\UAS, wordsRNA.1701.Scer\UAS clones.

The wing disc is absent in esgG66, sna1 double mutants, and the apical constrictions do not occur in the wing primordium cells. The haltere discs are similarly affected, but leg discs are unaffected. There is no sign of cell death in the prospective wing disc of the double mutant embryo. The mutant phenotypes can be rescued by either snahs.PF or esghs.PF.

shghs.PU; esgG66 embryos heat shocked twice also exhibit fused trachea.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Excision of the P{enG} element can revert the mutant phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (28)