Fig. 2. Ttrap knockdown with higher MO dose induces gastrulation defects.
(A,B) TtrapMO embryos (B) with thickened germ ring at
shield stage and a less distinct shield (arrowheads) than control (A). Animal
views, dorsal on top (gr, germ ring; sh, shield). (C-F) ttrap
is essential for CE movements. papc/myod-marked paraxial
mesoderm cells fail to converge close to the midline in TtrapMO
embryos (D,F). Dorsal-posterior views, tailbud stage. Double-headed arrows
depict width between cells spanning the midline. (G-I) ttrap
is required during epiboly. (G) Control embryo (3 ss) showing blastopore
closure (red arrowhead) and normal head with polster (blue). (H,I)
TtrapMO embryos (3 ss) showing varying degrees of severity with
respect to epibolic movements. (H) TtrapMO embryo displaying mild
epiboly defect (red arrowheads), which shows only slightly open blastopore and
relatively normal head morphology with polster (blue). (I) TtrapMO
embryo with more severe epiboly defect and larger open blastopore (red
arrowheads). Downward spread of blastoderm cells only covers 80% of yolk cell;
many of these embryos lyse shortly after; head region severely reduced in size
with polster missing (blue arrowhead). The combination of CE and epiboly
defects leads to severely truncated embryos. Blue dashed arrows and
semi-circle depict embryo length and angle between anterior-posterior (AP)
ends. Lateral views, dorsal to the right. (J,K) Live
controlMO versus TtrapMO embryo, 24 hpf. The morphant
embryo displays AP-axis truncation, microcephaly and micropthalmia.