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General Information
Symbol
Dmel\bru1QB
Species
D. melanogaster
Name
FlyBase ID
FBal0000707
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
aretQB72, AretQB
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C12299208T

Amino acid change:

Q404term | aret-PA; Q610term | aret-PB; Q161term | aret-PD; Q404term | aret-PE; Q404term | aret-PF; Q610term | aret-PG; Q373term | aret-PH; Q373term | aret-PI; Q373term | aret-PJ; Q373term | aret-PK

Reported amino acid change:

Q404term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: Q404term.

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

The indirect flight muscle (IFM) fibers of day 1 aretPD/aretQB mutant adults begin to thin and rupture close to their thoracic attachment sites. Additionally, the sarcomeres appear too short and are sometimes lost. Myofibrils are variable in diameter and often hollow, in contrast to dense, regular myofibrils in wild type. A few days after eclosion, generally all IFM fibers are ruptured and the myofibrils entirely lose their sarcomeric organisation. The tubular leg muscles do not display any obvious phenotypes.

aretQB mutants exhibit 'pseudo' egg chambers that contain ill-differentiated germline cysts.

In aretPA/aretQB adult females, oogenesis proceeds normally until stage 4 - meiosis and mitosis of germ cells occurs normally and nurse cells become enlarged an polyploid. But during stage 4, when mitosis of germ cells is over in wild-type, in around 20% of cysts the nurse cells condense their chromosomes and form large mitotic spindles.

Egg chambers from aretQB/aretQB females contain far greater thean the normal 16 germ cells, and these germ cell fail to become polyploid. Marker analysis suggests that these germ cell fail to exit mitosis at stage wild-type germ cells do.

Nuage does not appear disrupted in homozygous pseudo-egg chambers.

Oogenesis arrests at stage 6/7 in aretPD/aretQB females, although an oocyte is specified. Oogenesis arrests at stage 2 in homozygous females. Cysts form, but no oocyte is specified, and individual cysts sometimes contain more than 16 germline cells. Cytokinesis is complete within the cyst; there are no ring canals and the fusome appears as dots.

74% of embryos derived from heterozygous female hatch.

Germline cells in 70% of ovarioles from three to five day old adult aretQB females are arranged in small clusters within elongated germaria, These cells have not differentiated as nurse cells. The remaining 30% of ovarioles contain germaria that produce pseudo egg chambers comprised of fully encapsulated yet undifferentiated germline cells. The undifferentiated cells clusters within both the elongated germaria and the pseudo egg chambers contain germline cells ranging in number from single cells to more than 70 cells per cluster. Apoptotic cell death is not readily apparent in mutant ovarioles. Germline cells in mutant ovarioles undergo complete cytokinesis, but never form ring canals. No fusome is present in these cells, tiny and mispositioned spectrosome remnants are seen. Germline development in mutants pre-oogenesis is wild-type. When aretQB germ-line clones are made, the resulting pseudo-egg chambers are never mosaic, being entirely mutant or entirely wild-type. Somatic clones in the follicle cells, have no effect on the egg chamber. Germline development in mutants pre-oogenesis is wild-type.

Oogenesis is arrested in germarial stages in hemizygous females.

A number of small egg chambers in which the follicle cells secrete a tiny round chorion around the germline.

Homozygous females usually have a number of egg chambers in their ovaries in which the nurse cells and oocyte never seem to develop beyond stage 2 or 3 of oogenesis, but the follicle cells nevertheless synthesize a tiny round chorion around the cysts.

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

bru1QB/bru1PD has ovary phenotype, enhanceable by S[+]/S1

NOT Enhanced by
Statement
Reference

bru1QB has egg chamber phenotype, non-enhanceable by bamhs.PO

Suppressed by
Statement
Reference

bru1QB/bru1PD has ovary phenotype, suppressible by Df(3R)M-Kx1/+

bru1QB/bru1PD has ovary phenotype, suppressible by eIF4E1S251D

bru1QB/bru1PD has ovary phenotype, suppressible by Lk6EP886/Scer\GAL4[-]/Lk6[+]

bru1QB/bru1PA has phenotype, suppressible by Df(3R)M-Kx1

bru1QB has ovary phenotype, suppressible by Df(3R)mbc-R1

bru1QB has ovary phenotype, suppressible by Lk6EP886/Scer\GAL4[-]/Lk6[+]

NOT suppressed by
Statement
Reference

bru1QB has egg chamber phenotype, non-suppressible by bamhs.PO

Enhancer of
Statement
Reference

bru1QB/aret[+] is an enhancer of embryonic/first instar larval cuticle & embryonic head phenotype of Scer\GAL4VP16.nos.UTR, osk3'UTR.UASp

bru1QB is an enhancer of embryo | anterior phenotype of oskbcd.3UTR.A7

Suppressor of
Statement
Reference

bru1QB/aret[+] is a suppressor of dorsal appendage phenotype of grk2E12

Other
Additional Comments
Genetic Interactions
Statement
Reference

Oogenesis arrests at about stage 3 in S1 aretPD/aretQB females and no oocyte is specified. Df(3R)M-Kx1 dominantly suppresses the ovary phenotype of aretPD/aretQB females; the arrest in oogenesis occurs later in the double mutants than in the single mutant females. Expression of Lk6EP886 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 enhances the ovary phenotype of aretPD/aretQB females (oogenesis arrests at 3), while in the absence of an Scer\GAL4 driver, Lk6EP886 suppresses the ovary phenotype of aretPD/aretQB females (oogenesis arrests at stage 9). The stage at which oogenesis arrests in aretQB homozygous females is extended to stage 3 or 4 when Lk6EP886 is present. aretPD/aretQB eIF-4ES251D ; Lk6EP886/+ females arrest oogenesis at the same stage (stage 9) as aretPD/aretQB ; Lk6EP886/+ females. eIF-4ES251D suppresses the aretPD/aretQB ovary phenotype, delaying arrest of oogenesis until stage 9. The oogenesis arrest phenotype of aretQB homozygous females is suppressed by Df(3R)mbc-R1. Ovarioles in aretQB/aretQB ; Dl9P/+ females form a single large egg chambers with many germline cells. The fusome appears as dots. Most egg chambers have more than 16 germline cells in aretQB/aretPD ; Dl9P/+ ovaries. Three classes of abnormal egg chambers are seen, which are present in roughly equal numbers. In the first class, a large number of germline cells of roughly equal size are enveloped by a single epithelium of follicle cells. The remaining two classes arise from partial fusion of separate cysts; no stalk cells can be detected and the follicle cell layers of different egg chambers remain in contact with each other. In the "anterior/posterior fusion" class, a well-defined linear organisation within individual ovarioles is maintained, and adjacent egg chambers are fused with each other at their anterior and posterior boundaries. In the "random fusion" class, egg chambers are positioned irregularly and can be closely apposed to multiple different egg chambers on lateral as well as on anterior and posterior surfaces. In both the partial fusion classes, each egg chamber contains an oocyte. In the anterior/posterior fusion class the oocyte is present at the posterior of the cyst and in the random fusion class the oocyte is either lateral or posterior relative to the overall polarity of the ovariole.

The penetrance and severity of embryonic cuticle patterning defects in osk3'UTR.Scer\UAS.P\T; Scer\GAL4nos.UTR.T:Hsim\VP16 embryos is enhanced by aretQB/+.

72% of embryos derived from BicC5/aretQB females hatch.

Heterozygosity for aretQB reduces the penetrance of dorsal appendage loss or fusion phenotypes in eggs laid by grk2E12/+ females, from 80% to 40%.

The addition of bamhs.PO to aretQB mutants has no effect on the egg chamber phenotype.

Embryos derived from a cross of wild-type males to females heterozygous for aretQB and also heterozygous for either apt41, apt167, apt09049, apttdf-PΔ3 or apttdf-PΔ4 occasionally have head defects (these defects are not seen in embryos derived from females singly heterozygous for aretQB, apt41, apt167, apt09049, apttdf-PΔ3 or apttdf-PΔ4). This phenotype is largely suppressed (except in the case of aretQB apt09049 double heterozygotes) if the females are also heterozygous for nosL7.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (18)