FlyBase Allele Report: Dmel\bur[UAS.cLa]

General Information

Symbol

Dmel\bur^UAS.cLa

Species

D. melanogaster

Name

Saccharomyces cerevisiae UAS construct a of Long

FlyBase ID

FBal0193130

Feature type

allele

Associated gene

Dmel\bur

Associated Insertion(s)

Carried in Construct

P{UAS-bur.L}

Key Links

Transgenic product class

cDNA

(Long et al., 2006)

wild_type

(Long et al., 2006)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

cDNA

(Long et al., 2006)

wild_type

(Long et al., 2006)

Mutagen

in vitro construct

(Long et al., 2006)

Progenitor genotype

Carried in construct

P{UAS-bur.L}

Cytology

Description

UASt regulatory sequences drive expression of a full length bur cDNA (a 3.3kb fragment from EST RE18382).

(Long et al., 2006)

Allele components

Component

Use(s)

Regulatory region(s)

UASt

binary expression system - regulatory region

Encoded product / tool

bur

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

Expression of bur^Scer\UAS.cLa under the control of Scer\GAL4^GMR.PF does not result in eye defects.

(van der Knaap et al., 2010)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has visible phenotype, enhanceable by Bre1[+]/Bre1^kim1

(van der Knaap et al., 2010)

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has visible phenotype, enhanceable by Bre1^GD5127, Scer\GAL4^GMR.PF

(van der Knaap et al., 2010)

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has visible phenotype, enhanceable by EcR^V559fs

(van der Knaap et al., 2010)

Suppressed by

Statement

Reference

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has visible phenotype, suppressible | partially by EcR^A483T

(van der Knaap et al., 2010)

Other

Statement

Reference

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has visible phenotype

(van der Knaap et al., 2010)

Bre1[+]/Bre1^kim1, Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has partially lethal - majority die phenotype

(van der Knaap et al., 2010)

Phenotype Manifest In

Enhanced by

Statement

Reference

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has eye phenotype, enhanceable by Bre1[+]/Bre1^kim1

(van der Knaap et al., 2010)

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has eye phenotype, enhanceable by Bre1^GD5127, Scer\GAL4^GMR.PF

(van der Knaap et al., 2010)

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has eye phenotype, enhanceable by EcR^V559fs

(van der Knaap et al., 2010)

Suppressed by

Statement

Reference

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has eye phenotype, suppressible | partially by EcR^A483T

(van der Knaap et al., 2010)

Other

Statement

Reference

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has eye phenotype

(van der Knaap et al., 2010)

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has ommatidium phenotype

(van der Knaap et al., 2010)

Scer\GAL4^GMR.PF, Usp7^UAS.cKa, bur^UAS.cLa has interommatidial bristle phenotype

(van der Knaap et al., 2010)

Additional Comments

Genetic Interactions

Statement

Reference

Simultaneous co-expression of bur^Scer\UAS.cLa and Usp7^Scer\UAS.cKa under the control of Scer\GAL4^GMR.PF results in defects in the eye characterised by disorganized or missing ommatidia, loss of bristles and black necrotic patches.

Co-expression of Usp7^{C250A.Scer\UAS} and bur^Scer\UAS.cLa under the control of Scer\GAL4^GMR.PF does not result in eye defects.

Animals expressing bur^Scer\UAS.cLa and Usp7^Scer\UAS.cKa under the control of Scer\GAL4^GMR.PF and also heterozygous for Bre1^kim1 show strongly reduced viability. Surviving adults have a strongly enhanced mutant eye phenotype compared to animals expressing bur^Scer\UAS.cLa and Usp7^Scer\UAS.cKa under the control of Scer\GAL4^GMR.PF in an otherwise wild-type background.

Animals expressing bur^Scer\UAS.cLa under the control of Scer\GAL4^GMR.PF in a Bre1^kim1/+ background do not show eye defects.

Co-expression of Bre1^GD5127 enhances the eye defects caused by co-expression of bur^Scer\UAS.cLa and Usp7^Scer\UAS.cKa under the control of Scer\GAL4^GMR.PF.

EcR^V559fs enhances the eye defects caused by co-expression of bur^Scer\UAS.cLa and Usp7^Scer\UAS.cKa under the control of Scer\GAL4^GMR.PF.

EcR^A483T partially suppresses the eye defects caused by co-expression of bur^Scer\UAS.cLa and Usp7^Scer\UAS.cKa under the control of Scer\GAL4^GMR.PF.

(van der Knaap et al., 2010)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially rescues

bur^UAS.cLa/Scer\GAL4^elav-C155 partially rescues bur^e10

(Long et al., 2006)

bur^UAS.cLa/Scer\GAL4^GMR.PF partially rescues bur^e10

(Long et al., 2006)

Comments

Expression of bur^Scer\UAS.cLa under the control of Scer\GAL4^GMR.PF or Scer\GAL4^elav-C155 almost completely rescues the R-cell guidance defects seen in bur^e10 mutants.

Expression of bur^Scer\UAS.cLa under the control of Scer\GAL4^elav-C155 substantially rescues the pupal lethality of bur^e10 homozygotes.

(Long et al., 2006)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

bur^Scer\UAS.cLa

bur^UAS.cLa

Name Synonyms

Saccharomyces cerevisiae UAS construct a of Long

Secondary FlyBase IDs

References (2)

Report Sections

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