Sec5E10/Sec5E10 class IV da neurons in larval somatic clones manifest defects in dendritic growth (thinning of terminal dendrites, reduced total dendrite length and number of terminal branches, decreased number of dendritic intersections, varicosities).
Adults in which eye tissue has been made homozygous for sec5E10 during development (using the EGUF method) show complete eye ablation at both 25 and 18[o]C.
The frequency of successful tracheal cell fusions is decreased in embryonic dorsal branches of heterozygous sec5E10/+ embryos compared to wild-type.
In stage 16 homozygous sec5E10 embryos the dorsal longitudinal tracheal trunk is fused normally, but dorsal branches 1-5 fail to fuse.
sec5E10 mutant larvae display tracheal fusion defects in 22% of the examined tracheal dorsal branches.
sec5E10 homozygous clones induced in larvae at 25oC do not survive to pupal stage. However, they do survive if induced in larvae grown at 18oC and then shifted to 25oC after puparium formation. The localisation of some, but not all, markers of apical basal polarity is disrupted in cells in these clones in the developing notal epithelium at around 18 hours after puparium formation. In addition, a few cells in these clones have an abnormally small apex and disruption of more apical-basal polarity marker localisation - indicative of the beginning of delamination. Recycling endosomes in these mutant cells are enlarged.
Egg chambers in females containing homozygous germline clones lack membranes between the germ cells and have ring canals clumped together. In those egg chambers in which individual cells can be distinguished, the oocyte is often mispositioned anteriorly.
Females carrying sec5E10 germ-line clones do not lay any eggs. Examination of the ovaries of these flies reveals that oocyte development is arrested at stage 6. In sec5E10 homozygous germ cells in stage 6 egg chambers, actin filaments no longer separate the nuclei and the ring canals cluster together in the center of the egg chambers. In many instances the germ-cell nuclei are not separated by plasma membrane. Defects are also apparent much earlier: with many egg chambers fail to exit the germarium and ring canals clump together by stage 2. By stage 5 or 6, the follicle cell layer begins to disintegrate. In sec5E10 homozygous germlines, the oocyte is often mispositioned, as are the surrounding heterozygous polar follicle cells. Compound follicles with multiple germline cysts enclosed within a single follicle epithelium are also seen.
Homozygotes and sec5E10/Df(2L)tim-02 animals die within 96 hours of egg laying, as morphologically first instar larvae. The larvae hatch at the same time as their heterozygous siblings, at approximately 24 hours after egg laying (AEL) and their growth between 24 and 48 hours AEL is comparable to wild type. However, the mutant larvae do not grow after 48 hours AEL and remain as late first instar larvae, whereas by 96 hours AEL, wild-type larvae have progressed to the early third instar stage. In homozygous embryos, neuromuscular junctions develop with apparently normal morphology and the neuromuscular junctions of mutant embryos are size-matched to wild type until 48 hours AEL. Between 48 and 96 hours AEL, there is no growth of muscle 6 in the mutant, whereas it increases 6-fold in the wild type. The number of synaptic boutons at the neuromuscular junction of muscle 6 and 7 in the mutant shows no change between 48 and 96 hours AEL, whereas the number increases 2.5-fold in the wild type. Neural cells from the ventral nerve cord of sec5E10 larvae cultured in vitro show the same overall viability as wild-type larval neurons cultured in vitro. However, while in control cultures from wild-type larvae, 69% of neurons have extended neurites, neurites are scarce in sec5E10 cultures (only 4% of neurons cultured at 48 hours AEL extend neurites and less than 1% of healthy neurons in cultures made at 72 hours AEL have neurites). The few neurites that are present in sec5E10 cultures are significantly smaller than those in control cultures. The eye is completely ablated in mosaic animals in which the eye is homozygous for sec5E10. Females with homozygous germline clones do not produce eggs. Synaptic transmission at the neuromuscular junction persists between 48 and 96 hours AEL in mutant animals, and at 96 hours AEL, the evoked response is actually increased 2.5-fold over its amplitude at 48 hours AEL. The amplitude of type I spontaneous synaptic events (mEJCs) is unchanged in mutant animals at 48, 72 and 96 hours AEL compared to wild-type animals at 48 hours AEL.