FB2024_03 , released June 25, 2024
Allele: Dmel\fu52
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General Information
Symbol
Dmel\fu52
Species
D. melanogaster
Name
FlyBase ID
FBal0004885
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
fuJB3
Key Links
Genomic Maps

Mutagen
Nature of the Allele
Progenitor genotype
Cytology
Description

Defined by the absence of residues 29 to 37 in the N-terminal catalytic domain.

40bp deletion of genomic sequences 1002-1041, deletion of the 3' part of the first exon and 5' part of the first intron.

Mutation in the kinase domain. Class I fu allele, affects the catalytic domain but does not change the open reading frame.

Small deletion within putative kinase domain.

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

4 day old fu52 homozygous females, only 11% of egg chambers are tumorous, increasing to 35% at 10 days. This phenotype is stronger in fu50/fu52 females, in which 83% of egg chambers are tumorous ay 4 days, decreasing to 71% at 10 days. This is stronger than the phenotype in fu52/Df(1)fu-Z4 females, where around 50% of egg chambers are tumorous at 4 or 10 days. Tumorous follicles in these ovarioles consist of tens to hundreds of germ-line cells with small non-polyploid nuclei enveloped by a regular follicular epithelium. Marker expression studies and analysis of spectrosome morphology in tumorous cysts from fu52/Df(1)fu-Z4 animals suggest that these tumorous germ-line cells remain very immature and do not progress beyond the early cystoblast stage and may include germline stem cells (GSCs). However, the size of germline stem cell niches appears to be unnaffected - suggesting that these phenotypes are due to inceases in cystoblast-like cells outside of the niche. This increase is not due to increased cell division of germline stem cells in the niche - as assayed by scoring the percentage of GSCs in the niche undergoing mitosis in fu52/fu52 fu52/fu50 and fu52/Df(1)fu-Z4 adult females.

fu52 homozygous ovaries also contain egg chambers with increased numbers of germ cells that, based on marker expression and fusome morphology, have developed past the cystolast stage but are still more immature than normally found in female germline cysts outside of the germarium. There is some evidence of oocytes and nurse cell determination, but nurse cell and oocyte differentation appear to be blocked.

fu52/+ heterozygotes have a partial fusion of wing veins L3 and L4.

Homozygous females show a delay in the polar cell differentiation program. Restriction in the final number of polar cells is achieved by stage 5 in these females.

Mutant ovaries contain some egg chambers with more or less than the normal number of 16 germline cells. When an egg chamber contains less than 15 nurse cells, the complementary nurse cells are sometimes found in an adjacent egg chamber. In one case, an egg chamber containing two oocytes has been observed, indicating a multicyst egg chamber. In some cases the follicular epithelia of two adjacent egg chambers are apposed with no interfollicular stalk between them. The same ovariole can contain both normal and abnormal egg chambers. Degenerating egg chambers are seen. More dividing cells are seen in germarial regions 2 and 3 than in wild type. Mutant germaria show impaired encapsulation of the germline cysts by prefollicular cells, which results in some multicyst chambers. Interfollicular stalk cells do appear to be specified in the mutant germaria, but they are unable to fulfill their role in budding off of individual egg chambers. When stalk-like structures are seen between egg chambers they have an abnormal morphology, consisting of aggregates of round cells arranged in a ball shape (instead of the wild-type linear arrangement of 5-7 oval shaped cells). There is a delay in polar follicle cell specification. Clones induced in the somatic stem cells of the ovarioles can result in long, disorganised stalks within the ovariole, from which egg chambers show an off centre attachment. In most cases, these stalks are composed of fu+ cells, while the mutant cells are found as part of the follicular epithelium of adjacent chambers.

Mutants show fusion of wing veins L3 and L4 both proximally and distally, with intervein tissue remaining between the two veins in the medial part of the wing.

Weak wing phenotype (wing phenotype - veins L3 and L4 fused proximally), weak viability phenotype - ratio of the number of fused flies to wild type in fu/+ X fu/Y is 0.75-1.0; strong fecundity phenotype - ratio of eggs laid by fu/fu versus fu/+ sisters is 0-0.1.

Weak wing phenotype. Weak viability phenotype.

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

fu52 has ovariole phenotype, suppressible by Su(fu)LP/Su(fu)LP

fu52 has ovariole phenotype, suppressible by cos[+]/cos1

fu52 has phenotype, suppressible by Su(fu)LP

Additional Comments
Genetic Interactions
Statement
Reference

Hsap\fuScer\UAS.Δ77-98; Scer\GAL4ptc-559.1 enhances the partial fusion of wing veins L3 and L4 seen in fu52 flies.

When in combination with Su(fu)LP heterozygotes individuals display a partially suppressed fu phenotype. When in combination with cos3 individuals display no cos phenotype.

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

Class I mutation based on interaction with Su(fu)LP, suppression of embryonic and adult phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (12)