Table 2:
spint1a displays genetic interaction with epcam, but not with cdh1 (E-cadherin), in the developing epidermis, and spint2 with cdh1, but not with epcam, in the developing hatching gland.
| MO knock down | epidermal aggregates | scattered HGCs |
HGCs loss |
hatching defect |
|---|---|---|---|---|
| cdh1 low | − | − | − | − |
| epcam low | − | − | − | − |
| spint1a full | +++ | − | − | − |
| spint1a low | − | − | − | − |
| spint1a low + cdh1 low | − | − | − | − |
| spint1a low + epcam low | +++ | − | − | − |
| spint2 full | − | +++ | +++ | +++ |
| spint2 low | − | − | − | − |
| spint2 low + cdh1 low | − | +++ | + | ++ |
| spint2 low + epcam low | − | − | − | − |
Full or low amounts of morpholino oligonucleotides (MOs) were injected for complete or partial gene knock down. Embryos were assayed for the development of epidermal aggregates at 24 hpf, applying live imaging, and the development of a scattered hatching gland cell (HGC) phenotype at 34 hpf and hatching gland cell loss at 44 hpf, applying ctslb WISH, as well as their hatching rate at 72 hpf. −, no defects; +, weak defects; ++, intermediate defects; +++, strong defects. For spint2 – cdh1 interaction, compare with Figure 9D,J,K.