Src64B^Δ17/Src64B^ko females lay significantly fewer eggs than wild type. 43% of these eggs hatch.

Ring canal diameter in homozygous egg chambers significantly smaller than wild type. Nurse cell fusion is seen in the mutant egg chambers.

Homozygous embryos derived from homozygous females show defects during cellularisation. The microfilament rings show significantly more deviation from circularity than in wild-type embryos during both early and late cellularisation.

Src64B^Δ17 females lay fewer eggs than wild-type females and under 5% of these eggs hatch.

The egg chambers of Src64B^ko females contain aberrantly small ring canals (on average 6.8μm diameter vs 9.1μm in wild-type females).

Src64B^Δ17 egg chambers have aberrant cell numbers. The total germ cell number is usually a multiple of the wild-type number of 16; for example, Src64B^Δ17 egg chambers have been observed with 30 nurse cells and 2 oocytes and also with 60 nurse cells and 4 oocytes. Src64B^Δ17 egg chambers contain the wild-type number of ring canals and nurse cell nuclei indicating that the aberrant cell number phenotype is not due to changes in germ cell proliferation.

Src64B^Δ17 egg chambers derived from single Avic\GFP-labelled germline cyst clones contain both Avic\GFP-labelled and unlabelled cells, suggesting that cells from more than one cyst have been packaged into a single egg chamber.

Src64B^Δ17/Src64B^ko transheterozygous females show egg chamber packaging defects.

Src64B^Δ17 nurse cells exhibit normal morphology. Gaps in the follicle cell layer and follicle cell polarity defects are not observed and polar and stalk cell differentiation is normal in Src64B^Δ17 ovarioles. Src64B^Δ17 egg chambers are always separated by stalks, even when egg chambers are mispackaged.

In Src64B^Δ17 germaria, cysts with aberrant cell numbers are frequently observed and, in rare cases, cell are separated from the rest of the cyst. The follicle cells in these germaria extend projections and migrate to fully surround the germline cysts. The penetrance of Src64B^Δ17 packaging defects within germaria parallels that observed in vitellaria.

Src64B^Δ17 mutant ovaries have multiple defects in oogenesis, including apoptosis, the fusion of neighbouring egg chambers, mislocalized oocytes and an absence of stalk cells. Src64B^Δ17 mutants can, on rare occasions, contain compound egg chambers that have two oocytes, each with four ring canals. Src64B^Δ17 ovaries can contain binucleate nurse cells at all stages of oogenesis. Many of the oogenesis defects seen in Src64B^Δ17 mutants appear to be connected to defects in the cytoskeleton. For example, F-actin is unevenly distributed along cell membranes within the egg chamber, causing an abnormal cell shape. Karyosome formation, which usually overlaps with G-actin accumulation, occurs later than in wild type and karyosomes are not always compact and spherical, indicating defects in chromatin condensation. Fusomes have greater levels of F-actin than wild type and appear abnormal in all mutants. Finally, the microtubule-dependent transport of proteins from the nurse cells to the oocyte appears to be affected in Src64B^Δ17 mutants.

In the ovarioles of Src64B^Δ17 mutants, 30% contain fused egg chambers at 18^oC; this value drops to 15% at 25^oC and 8% at room temperature. Germline clones for Src64B^Δ17 have similar morphology (18^oC - 35%; 25^oC - 10%). After several generations, the fertility of Src64B^Δ17 homozygous lines increases and the number and severity of egg chamber defects decreases.

In cellularizing Src64B^Δ17 mutant embryos, the furrow canals are less rounded, and adjacent furrow canals extend to different depths in the embryo, giving the cellularization front a wavy, slack appearance as if it were no longer under tension. In these embryos the microfilament rings that can be seen from the surface during cellularization are not rounded, as in wild-type, but instead are irregular in shape and sometimes sharply angular. However, membrane insertion during cellularization still proceeds in these embryos. The depth of membrane invagination and the dynamics of cellularization front ingression is similar to that of wild-type embryos.

The morphology of nurse cell ring canals in Src64B^Δ17/Src64B^Δ17 flies is abnormal. Electron microcopy shows that at stage 6, ring canals from wild-type and mutant flies have roughly similar morphologies (although mutants have slightly thicker actin bands). However, by stage 10A the ring canals in mutants have distinct differences with wild-type. Light microscopy and actin localisation show that they are significantly narrower than in wild-type, and have a much more concave rim. Electron microscopy shows that the ring canal F-actin remains continuous with no separation into cables as in wild-type; unlike wild-type, the electron-dense material of the outer rim also remains continuous, and folds dramatically into a pointed shape, rather than remaining flat. The rate of actin monomer exchange with actin filaments of the nurse cell ring canals is much slower in Src64B^Δ17 homozygotes than in wild-type.

phl^Su2/Y ; Src64B^Δ17/Src64B^Δ17 males show semi-lethality. The surviving males have eyes that are slightly small and rough.

Homozygous females have reduced fertility; eggs laid by these females hatch at a reduced frequency (20.0%) compared to wild-type. Homozygous females show a defect in cytoplasmic transfer during oogenesis. Stage 10A egg chambers sometimes contain fewer than 15 ring canals. Fusion of nurse cells is sometimes seen, and, rarely, detached ring canals are seen within the cytoplasm of the fused nurse cells.

Homozygotes show defects in fertility and a small ring canal phenotype.

Homozygous females lay eggs that are variably reduced in size, and have a reduced hatching rate of 35% compared to wild-type. Ring canals are smaller than normal.

Src64B^Δ17 has semi-sterile phenotype, enhanceable by Btk^e482

Src64B^Δ17 has lethal | embryonic stage | maternal effect | recessive phenotype, enhanceable by Btk^k05610

Src64B^Δ17 has lethal | embryonic stage | maternal effect | recessive phenotype, enhanceable by Btk^k00206

Raf^Su2, Src64B^Δ17 has partially lethal - majority die phenotype

Raf^Su2, Src64B^Δ17 has visible phenotype

Df(3L)GN24/Src64B^Δ17, Raf^Su2 has lethal phenotype

Src64B^Δ17 has egg chamber phenotype, enhanceable by Btk29A[+]/Btk^k05610

Src64B^Δ17 has egg chamber phenotype, enhanceable by Btk29A[+]/Btk^k00206

Src64B^Δ17 has nurse cell ring canal phenotype, enhanceable by Btk^e482

Src64B^Δ17 has nurse cell ring canal phenotype, enhanceable by Df(2L)TE29Aa-14

Src64B^Δ17 has nurse cell ring canal phenotype, enhanceable by Btk^k00206

Src64B^Δ17/Src64B^ko has egg chamber phenotype, suppressible | partially by Csk[+]/Csk^unspecified

Src64B^Δ17 has nurse cell ring canal phenotype, suppressible by Csk[+]/Csk^unspecified

Src64B^Δ17 has egg chamber phenotype, suppressible by Csk[+]/Csk^unspecified

Src64B^Δ17 has karyosome phenotype, non-suppressible by mei-W68¹

Src64B^Δ17 has karyosome phenotype, non-suppressible by mei-41^D3

Src64B^Δ17 has furrow canal phenotype, non-suppressible by Df(3R)tll-e

Src64B^Δ17 has plasma membrane | embryonic stage 5 phenotype, non-suppressible by Df(3R)tll-e

Src64B^Δ17 has actin filament | embryonic stage 5 phenotype, non-suppressible by Df(3R)tll-e

Src64B^Δ17 is a non-enhancer of ommatidium phenotype of csw^lf

Src64B^Δ17/Src64B[+] is a non-enhancer of phenotype of ct^L188

Src64B^Δ17/Src64B[+] is a non-enhancer of phenotype of ct^C145

Src64B^Δ17 is a non-enhancer of phenotype of ct^C145

Raf^Su2, Src64B^Δ17 has eye phenotype

Raf^Su2, Src64B^Δ17 has ommatidium phenotype