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. 2018 Dec 12;145(24):dev168922. doi: 10.1242/dev.168922

Fig. 5.

Fig. 5.

plekhg5 is required for endogenous blastopore lip formation. (A) Schematic of the genomic regions of the L and the S alloalleles of plekhg5 that are targeted by the SB MOs. The positions of the primers used for RT-PCR analysis of splicing efficiency are shown. (B,C) Both SB-MO1 and SB-MO2 efficiently block splicing of both L and S alloalleles, as indicated by the presence of intron-retention products in plekhg5 morphant embryos. The primer pairs used in the PCR reactions are indicated in parentheses. (D) plekhg5 SB MOs prevent formation of the blastopore lip at the sites of its injection. (E) plekhg5 SB MOs do not alter mesodermal cell fates, though the movements of the prechordal tissue (gsc-expressing, purple) and the trunk mesoderm (bra-expressing, cyan) are affected. (F) The blastopore lip defects induced by the SB MOs (25 ng) can be rescued with low doses of co-expressed plekhg5 RNA (25-50 pg). (G) plekhg5 SB MOs (25 ng) block ectopic blastopore lip induction by activin (5 pg) without affecting activin-dependent mesodermal induction. Numbers in each image indicate embryos exhibiting the ectopic blastopore lip defects or ectopic blastopore lips over the total number of embryos.