FB2024_04 , released June 25, 2024
Allele: Dmel\COX5Atend
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General Information
Symbol
Dmel\COX5Atend
Species
D. melanogaster
Name
tenured
FlyBase ID
FBal0217453
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
CoVatend
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

A 56bp deletion close to the translational start site of CoVa.

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
Detailed Description
Statement
Reference

Expression of COX5Atend under the control of Scer\GAL4109(2)80 results in slight shortening of the dendritic arbor in the class IV ddaC neurons in third instar larvae.

Mutant embryos do not show defects in the somatic muscle pattern.

CoVatend mutant eye disc clones exhibit a disruption in cell division as mitotic waves are disrupted, as shown by a failure to incorporate BrdU.

COX5Atend homozygous somatic clones induced in a 'minute' background in the eye have a 'glossy' phenotype - the mutant tissue appears smooth due to lack of lens development. Cell division in these clones in the eye disc is normal until the late third instar. However, the second mitotic wave of cell division (posterior to the furrow) fails to occur in mutant cells and at the first mitotic wave (just anterior to the furrow) entry into S-phase is slower than in wild-type. Despite this, ommatidial patterning and differentiation proceed relatively normally in these clones - recruitment to ommatidial pre-clusters occurs normally, although some perturbation of the spacing and orientation of clusters is evident.

FACS analysis of dissociated wing discs containing COX5Atend homozygous clones shows that a greater fraction of COX5Atend homozygous cells are in G1 for wild-type cells. Mutant cells are also about 13% larger, on average, than wild-type. BrdU incorporation occurs normally in these clones if they are small (a few cells only), but is largely absent in larger clones. These larger clones are smaller than their adjacent twin-spot.

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

The shortening of the dendritic arbor in class IV ddaC neurons observed in third instar larvae expressing COX5Atend under the control of Scer\GAL4109(2)80 can be rescued by co-expression of PPP1R15Scer\UAS.cMa.

A p5311-1B-1 background suppresses the cell division disruption found in CoVatend mutant eye disc clones.

A Pros261 background suppresses the cell division disruption found in CoVatend mutant eye disc clones. Interestingly, the glossy adult eye phenotype of CoVatend mutant clones is also significantly suppressed.

An ago1 heterozygous background suppresses the CoVatend mutant clone adult eye phenotype.

A lin19EX or Cul-3gft2 heterozygous background does not suppress the disruptions in cell division seen in CoVatend mutant eye disc clones.

The 'glossy' eye phenotype due to CoVatend homozygous clones is largely suppressed if the clones are also homozygous for SNF4AγKG00325 or if the clones are generated in a p5311-1B-1 homozygous background. The cell cycle defects seen in CoVatend homozygous clones in the eye disc are also suppressed by in these backgrounds.

The 'glossy' eye phenotype due to CoVacl-R3 homozygous clones is largely suppressed if the clones are also homozygous for SNF4AγKG00325 or if the clones are generated in a p5311-1B-1 homozygous background. The cell cycle defects seen in CoVacl-R3 homozygous clones in the eye disc are also suppressed by in these backgrounds.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Name Synonyms
tenured
Secondary FlyBase IDs
    References (7)