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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
l(3)j2B10, D14-3-3εl(3)j2B10
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Insertion of a P{lacW} element within the first intron.

Insertion components
Product class / Tool use(s)
Encoded product / tool
Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Homozygous females lay very few eggs.

Pole cells appears dispersed all over the embryo in homozygous 16-18 hours embryos with the number of pole cells per gonad being reduced compared to wild type at stages 8 and 11-12.

Homozygous and 14-3-3εj2B10/14-3-3εNP1301 embryos show highly penetrant axon guidance defects in the ISNb and SNa axons.

No retinal phenotypes are seen in 14-3-3εj2B10 mutant flies.

The eyes of heterozygous 14-3-3εj2B10 flies appear normal.

Homozygous 14-3-3εj2B10 mutants are smaller than their isogenic siblings, as measured by whole body size, body weight, and wing size.

Trans-heterozygous 14-3-3εj2B10/14-3-3εex4 mutants are smaller than their isogenic siblings, as measured by body weight.

Both homo- and heterozygous 14-3-3εj2B10 mutants display increased sensitivity to ultraviolet irradiation induced apoptosis.

Mean and maximum lifespan of 14-3-3εj2B10 heterozygotes is significantly higher than that of sibling controls.

Homozygotes show 75% viability. 14-3-3εex4/14-3-3εj2B10 animals show 71% viability.

Homozygous adults have smaller wings than control flies. 25% of homozygotes have defects in the anterior crossvein, while 75% have defects in the posterior crossvein.

26.7% of 14-3-3εex4/14-3-3εj2B10 adults have defects in the anterior crossvein, while 82.4% have defects in the posterior crossvein.

In 14-3-3εj2B10 homozygotes or 14-3-3εj2B10/Df(3R)P14 females most egg chambers lack a differentiated oocyte: both of the nurse cells with four ring canals develop as nurse cells. The same phenotype is caused by 14-3-3εj2B10 germ-line clones, but not 14-3-3εj2B10 somatic clones in the ovarian follicle cells. The microtubule organizing center which is visible in the posterior of the prospective oocyte as early as stage 2 in wild-type, is absent from 14-3-3εj2B10 mutants at this stage. The centrosomes do not undergo the anterior-to-posterior movement and eventually diffuse away as this cell exits meiosis and adopts a nurse cell fate. In 14-3-3εj2B10 mutant egg chambers where oocyte specification does occur, marker analysis at stage 10 shows a partially penetrant oocyte polarization phenotype, although migration of the oocyte nucleus occurs normally. These oocytes also show defects in microtubule organization.

Embryos derived from a cross of 14-3-3εj2B10/Df(3R)Cha7 females to 14-3-3εj2B10/Df(3R)Cha7 males progress through the first 13 mitotic cycles and cellularise without obvious defects. Cells enter mitosis 14 prematurely compared to wild type so that the division pattern of mutant embryos in gastrulation is more advanced than in wild-type embryos of similar gastrulation but is similar to wild-type embryos of more advanced gastrulation. The entire schedule of mitosis is advanced without disrupting the relative order of mitosis in different positions within the embryo. The rate of germ-band elongation is indistinguishable from wild type. Mutant embryos do not show a delay of entry into mitosis 14 after irradiation, in contrast to wild-type embryos.

In the absence of irradiation, 14-3-3εj2B10 animals have a normal external appearance, normal imaginal disc morphology and normal numbers of mitotic cells in the discs. After irradiation, the number of mitotic cells in 14-3-3εj2B10 discs is greater than the number found in irradiated wild-type discs.

Homozygotes have normal eyes but are sterile. 14-3-3εS-696/14-3-3εj2B10 flies have rough eyes and a low penetrance of missing photoreceptors in the ommatidia.

Germline clones produce normal eggs with no cuticle development.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Enhancer of
Suppressor of
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
Suppressor of
Additional Comments
Genetic Interactions

Expression of one copy of Sema-1aScer\UAS.cYa under the control of Scer\GAL4how-24B in embryos that are also heterozygous for 14-3-3εj2B10 results in axon guidance defects in the ISNb and SNa nerves, resulting in reduced muscle innervation.

The axon guidance defects in the central nervous system which are caused by expression of plexAScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PU are enhanced if the embryos carry 14-3-3εj2B10.

The ISNb and SNa axon guidance defects seen in 14-3-3εj2B10/14-3-3εNP1301 embryos are significantly suppressed by expression of either Ras64BVal14.Scer\UAS, ifScer\UAS.cUa or mewScer\UAS.cWa under the control of Scer\GAL414-3-3ε-NP1301.

The eye overgrowth phenotype caused by expression of ykiScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF is enhanced by 14-3-3εj2B10/+.

The dwarf phenotype of homozygous 14-3-3εj2B10 mutants is reverted in a foxo21 mutant genetic background.

The lifespan of 14-3-3εj2B10/+, foxo21/+ double heterozygous flies is similar to wild-type levels.

Follicular epithelium morphogenesis is normal in 14-3-3ζP1188/14-3-3ζP1375 ; 14-3-3εj2B10/+ egg chambers up to stage 4, but the follicle cells subsequently lose their regular cuboidal shape.

The penetrance of the oocyte to nurse cell transformation phenotype seen in 14-3-3εj2B10 germ-line clones (80% n=106) is dominantly enhanced to 100% by 14-3-3ζP1188. In 14-3-3εj2B10 mutant egg chambers that develop an oocyte, the penetrance of oocyte polarization defects in oocytes at stage 10 is dominantly enhanced by par-1W3. Many 14-3-3ζP1188 germ-line clones in 14-3-3εj2B10/+ females have defects in oocyte specification and polarization.

R8 photoreceptor cells fail to form in EgfrE1/+ ; 14-3-3εj2B10/Df(3R)P14 eye discs.

Homozygotes but not heterozygotes suppress the Ras85DV12.sev rough eye phenotype. 14-3-3ζX1/+ 14-3-3εj2B10/14-3-3εj2B10 or 14-3-3ζ2.3/+ 14-3-3εj2B10/14-3-3εj2B10 flies have slightly roughened eyes, a low penetrance of missing photoreceptors and a gap in the posterior crossvein of the wings in more than 50% of cases.

Xenogenetic Interactions

One copy of 14-3-3εj2B10 suppresses the retinal phenotype seen when Hsap\HTT128Q.1-336.Scer\UAS is expressed under the control of Scer\GAL4GMR.PU.

One copy of 14-3-3εj2B10 suppresses the retinal phenotype seen when Hsap\ATXN182Q.Scer\UAS is expressed under the control of Scer\GAL4GMR.PU.

Complementation and Rescue Data
Images (0)
Stocks (2)
Notes on Origin

Complements: repo03702. Complements: l(3)0582205822. Complements: MED17s2956.

The rough eye and missing photoreceptor cell phenotype of 14-3-3εS-696/14-3-3εj2B10 flies is reverted by mobilisation of the P-element in 14-3-3εj2B10. The recessive lethality of the 14-3-3εj2B10 chromosome is not associated with the P-element insertion.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (12)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (19)