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. Author manuscript; available in PMC: 2022 Jul 1.
Published in final edited form as: Dev Biol. 2021 Mar 5;475:21–29. doi: 10.1016/j.ydbio.2021.02.014

Fig. 5.

Fig. 5.

In vivo analysis of Lv-kirrelL cMO. Left panels- Living embryos (24 hpf) viewed with differential interference contrast (DIC) and polarization (POL) optics. Control embryos (+cMO, −UV) developed complete skeletons that contained elongated, paired body rods (BR) and postoral rods (PO). Decaging of the Lv-kirrelL cMO at the 1-cell stage (+cMO, +UV; lateral view) resulted in highly reduced skeletons, phenocoping the effects of the non-caged form of the MO (Ettensohn and Dey, 2017). The arrowhead indicates one small, birefringent spicule rod that formed in this embryo. Top right panels- Late gastrula stage embryos (16 hpf) immunostained with monoclonal antibody (mAb) 6a9, which specifically labels PMCs (Ettensohn and McClay, 1988). In control embryos (+cMO, −UV), PMCs became aligned in strands and their cell bodies were joined by a prominent filopodal cable (arrow). Decaging of the Lv-kirrelL cMO at the 1-cell stage (+cMO, +UV) blocked PMC fusion, as indicated by the scattered arrangement of the cells and absence of a filopodial cable. Bottom right- Quantification of phenotypes of embryos injected with the non-caged or caged form of Lv-kirrelL MO. Embryos injected with cMO were irradiated at the 1-cell stage. Morphant phenotypes were scored at 24 hpf as shown in Fig. 3.