The centrosomes of egl1/egl2 mutant cysts migrate along the fusome and accumulate in a single cell in late region-2b and region-3 cysts (as occurs in wild type) but they do not move to the posterior of this cell and remain associated with the remnants of the fusome (in contrast to wild type). The cell that accumulates the centrosomes contains the largest portion of the degenerating fusome.
The synaptonemal complex (SC) forms with equal intensity in all 16 cells of the germline cyst in early region 2a in egl2/egl1 females. All of the cells appear to be fully synapsed, but the SC looks somewhat thinner than in wild type. The SC is not maintained, however, and disappears before the cysts reach region 2b. The 16 cells form nurse cells.
16 cell vitellarial cysts cease to enlarge partway down the vitellarium and are eventually phagocytosed. Cyst production dynamics are normal. All 16 nuclei in a cyst enter meiosis; the chromatin condenses and synaptonemal complex is present. Later all 16 lose the synaptonemal complex and assume nurse cell characteristics. Cell shape changes within the cyst are normal as the cysts pass down the germarium. Synaptonemal complex is of normal width and is apparently normal in substructure, but throughout pachytene it maintains the extreme thinness typical of wild-type synaptonemal complex during zygotene. Most "pachytene" nuclei in egl mutant cysts have zygotene numbers of synaptonemal complex segments as well as zygotene thinness. The nuclei do mount both early and late recombination nodules, at normal positions within the germarium. Number of recombination nodules per nucleus is comparable to that in wild type pro-oocyte. The onset of cytoplasmic flow is delayed. In mid-vitellarium the 16 cells remain the same size. Ring canals frequently do not enlarge as much as they should, and are more likely to be lacking their inner lining than in wild type. The fusome is apparently normal. Centrioles and mitochondria orient normally. Centriole replication continues. Mitochondria indicate that the ring canals may be unusually difficult to pass through.
Oogenesis is blocked at an early stage, oocyte fails to differentiate properly and all 16 cells develop as nurse cells.
16 nurse cells in a follicle rather than 15 and an oocyte. Follicle breaks down after stage 7. Normal morphological markers for polarity, such as gradient in size of nurse cell nuclei, can be identified in mutant follicles, but their spatial organisation is disturbed. Up to stage 5 the relative position of the presumptive ooocyte is normal, after stage 5 it is often found in aberrant positions: mis-positioning is correlated with aberrant pattern of extracellular ionic currents. Mutant follicles have differentiating follicular epithelium in patches, whereas wild type only has such cells around the oocyte.
Abdominal defect: no eggs.
Egg chambers contain 16 nurse cells and no oocyte.
When transheterozygous with a deficiency, ovary size is no smaller than for the egl2 homozygote.