12-18% of 14-3-3ζ^P1188/14-3-3ζ^P2335 heteroallelic animals are escapers. They do not exhibit external defects or grossly aberrant behaviors, despite no 14-3-3ζ expression.

Border follicle cell migration is disrupted in mosaic egg chambers containing homozygous follicle cell clones.

Large homozygous follicle cell clones show dramatic defects in tissue organisation, forming multilayers of morphologically abnormal cells that often fail to encapsulate germline cysts properly. Smaller homozygous follicle cell clones that arise after epithelium formation have milder and less penetrant defects in morphology and polarity.

14-3-3ζ^P1188 germ-line clones do not exhibit defects in oocyte specification or polarization.

Flies rescued from lethality by 14-3-3ζ^LI.15.hs or 14-3-3ζ^LI.15.hs and 14-3-3ζ^LII.2.hs show a 25-30% decrement in olfactory learning, comparable to that of (rescued) 14-3-3ζ^2.3. The restoration of learning by the transgenes decays back to mutant levels 60-70 hr later.

Homozygous embryos show no apparent defects in the timing of mitotic cycle 14 and show delayed mitosis after irradiation (as occurs in wild type). 69 +/- 9% of mutant embryos derived from homozygous female germline clones fail to cellularise. 54/59 of the embryos have defects in cell division, including DNA bridges between telophase sister nuclei, asynchrony in division within a single embryo, free microtubule-organizing centres that are not associated with nuclei, loss of nuclei from the cortical monolayer of nuclei and larger than normal yolk DNA masses. Chromosome bridges interconnecting DNA masses are seen as early as telophase of the fourth embryonic mitosis. Mitotic spindles do appear to be formed in these embryos (as judged by the segregation of chromosome masses that are still linked by DNA bridges to opposite spindle poles), and attempts at the formation of mid-bodies are seen between segregating nuclei, despite the presence of chromosome bridges. Approximately 30% of embryos cellularise. These embryos have severe gastrulation defects.

Embryos do not exhibit a dorsal closure defect. The amplitude and frequency of endogenous excitatory junctional currents (EJCs) is reduced relative to wild type and the NMJ exhibits a transmission defect, the calcium dependence curve is shifted to the right indicating a higher level of external calcium is required to achieve the given level of secretion.

Embryos derived from homozygous female germline clones show a variable phenotype that is not significantly different whether or not the embryos contain a wild-type copy of 14-3-3ζ from the father. Approximately 50% of the embryos do not develop cuticles, and the remainder develop cuticles with various segmentation defects including missing and/or fused denticle bands. The Filzkorper appear normal. Approximately 50% of the embryos appear to stop development during the syncytial blastoderm stage, and contain many fewer nuclei compared to wild-type. Some of these nuclei appear fused. 18% of embryos carrying 14-3-3ζ^hbNRE.RpII15 and derived from homozygous 14-3-3ζ^P1188 female germline clones have a wild-type anterior region but are missing all or part of the posterior region. 56% of these 'anteriorly rescued' embryos have shortened Filzkorper.

Heterozygotes exhibit normal 3 minute memory performance. Odour avoidance (octanol and benzaldehyde) is normal.

14-3-3ζ^P1188 is an enhancer of nurse cell | ectopic | germline clone phenotype of 14-3-3ε^j2B10

14-3-3ζ^P1188 is an enhancer of oocyte | germline clone phenotype of 14-3-3ε^j2B10

14-3-3ε^j2B10, 14-3-3ζ^P1375/14-3-3ζ^P1188 has follicle cell phenotype

14-3-3ε^j2B10/14-3-3epsilon[+], 14-3-3ζ^P1375/14-3-3ζ^P1188 has follicle cell phenotype

14-3-3ε^S-1259, 14-3-3ζ^P1188 has oocyte | germline clone phenotype

14-3-3ε^j2B10, 14-3-3ζ^P1188 has oocyte | germline clone phenotype

14-3-3epsilon[+]/14-3-3ε^S-1259, 14-3-3ζ^P1188 has oocyte | germline clone phenotype

14-3-3ε^j2B10/14-3-3epsilon[+], 14-3-3ζ^P1188 has oocyte | germline clone phenotype