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General Information
Symbol
Dmel\gcmDN.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0179660
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-glideDN, UAS-gcmDN
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UAS sequences drive expression of a dominant-negative form of gcm that consists of the gcm DNA-binding domain (amino acids 1-390) fused to the en repressor domain (amino acid residues 1-304).

Allele components
Product class / Tool use(s)
Encoded product / tool
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
Detailed Description
Statement
Reference

Animals carrying gcmDN.Scer\UAS.T:en-Rep, Scer\GAL4srp.D.cCa and Scer\GAL80ts.αTub84B and raised at 18[o]C are viable and fertile.

Animals carrying gcmDN.Scer\UAS.T:en-Rep, Scer\GAL4srp.D.cCa and Scer\GAL80ts.αTub84B which have been raised at 18[o]C and then shifted to 29[o]C (the restrictive temperature for Scer\GAL80ts.αTub84B) during the first larval instar stage show a melanotic tumour phenotype at the third larval instar stage and die at the pupal stage. Temperature shift experiments show that the melanotic tumour phenotype is less severe (fewer larvae having fewer tumours) when Scer\GAL80ts.αTub84B is inactivated after the first larval instar stage, and no melanotic tumours are induced if Scer\GAL80ts.αTub84B is inactivated at the early third larval instar stage.

Animals carrying gcmDN.Scer\UAS.T:en-Rep, Scer\GAL4srp.D.cCa and Scer\GAL80ts.αTub84B which have been raised at 18[o]C and then shifted to 29[o]C during the first larval instar stage show a strong increase in lamellocyte production compared to controls when analysed at the third larval instar stage. The ratio of plasmatocytes compared to total hemocyte number is significantly decreased in these animals compared to the ratio in controls.

Animals carrying gcmDN.Scer\UAS.T:en-Rep, Scer\GAL4gcm-rA87.P and Scer\GAL80ts.αTub84B which are raised at 18[o]C are viable and fertile (at this temperature, Scer\GAL80ts.αTub84B is active and represses Scer\GAL4gcm-rA87.P).

No adults eclose when animals carrying gcmDN.Scer\UAS.T:en-Rep, Scer\GAL4gcm-rA87.P and Scer\GAL80ts.αTub84B are raised at 30[o]C (at this temperature, Scer\GAL80ts.αTub84B is inactive, allowing expression of gcmDN.Scer\UAS.T:en-Rep under the control of Scer\GAL4gcm-rA87.P).

Animals carrying gcmDN.Scer\UAS.T:en-Rep, Scer\GAL4gcm-rA87.P and Scer\GAL80ts.αTub84B which are raised at 18[o]C until the early second larval instar stage and then transferred to 30[o]C lack all migrating medulla neuropile glia when examined at the late third larval instar stage (other glial populations are present). These animals also show a complete loss of the "cup-like" clusters of glia that are normally seen in each thoracic hemineuromere (the leg neuropile glia). There are no defects in the gcm-positive neurons of the ventral nerve cord.

Expression of gcmDN.Scer\UAS.T:en-Rep, under the control of Scer\GAL4bi-omb-Gal4 results in R axon projection defects, suggesting that the differentiation of the lamina glia is compromised. The lamina is smaller than in wild-type and the morphology is defective. Expression of gcmDN.Scer\UAS.T:en-Rep, under the control of Scer\GAL4NP6099 results in a severe reduction in the number of dac-positive lamina cells. R axon projection to the presumptive lamina target field still occurs, although there are patterning defects.

In early stage 17 gcmDN.Scer\UAS.T:en-Rep; Scer\GAL4ptc-559.1 embryos, some ventral longitudinal muscles bypass their target tendon cells, cross the ventral midline and attach to muscles on the opposite side. This phenotype is not seen in gcmDN.Scer\UAS.T:en-Rep; Scer\GAL4sr-md710 flies.

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

The melanotic tumour phenotype caused by expression of gcmDN.Scer\UAS.T:Rep-en under the control of Scer\GAL4srp.D.cCa (the animals also carry Scer\GAL80ts.αTub84B which has been inactivated by shifting to the restrictive temperature) is completely suppressed in a hop2/Y background.

The melanotic tumour phenotype see in animals carrying gcmDN.Scer\UAS.T:Rep-en, Scer\GAL4srp.D.cCa and Scer\GAL80ts.αTub84B which have been raised at 18[o]C and then shifted to 29[o]C during the first larval instar stage is completely suppressed if they are also co-expressing one of upd1GD1158, upd3GD6811, Stat92EGD4492, domeGD14494 or hopGD9157.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
gcmDN.Scer\UAS.T:Rep-en
gcmDN.Scer\UAS.T:en-Rep
gcmDN.Scer\UAS
gcmDN.UAS
Name Synonyms
Secondary FlyBase IDs
    References (5)