Fig. 9

Knockdown of PaxA results in loss of cnidocytes. a The PaxA sp MO recognizes the I1E2 boundary which should cause skipping of exon 2, but the PaxA transcript could only be amplified from embryos injected with control morpholino (Ctrl MO). b The PaxC sp MO blocks the E1I1 boundary causing retention of intron 1. Both WT and morphant transcripts were amplified from PaxC MO-injected embryos. c–g Developing cnidocytes labeled with α-NCOL4 antibody in embryos injected with c control morpholino, d PaxA splice-blocking morpholino, e PaxA translation-blocking morpholino, f PaxC splice-blocking morpholino, and g PaxC translation-blocking morpholino. h Quantitative analysis of cnidocyte abundance in early-planula-stage embryos. Control morpholino-injected embryos exhibited wild-type abundance of cnidocytes, whereas PaxA sp morphants and PaxA tr morphants had significantly fewer (control MO: 9.11 ± 0.39, PaxA sp: 3.65 ± 0.63, PaxA tr: 4.90 ± 0.66; mean ± standard error). Both PaxC sp morphants and PaxC tr morphants exhibited an increase in cnidocyte abundance, albeit with a small effect size (PaxC sp: 10.58 ± 0.68, PaxC tr: 12.44 ± 0.47). i PaxA mRNA partially rescues SoxB2 ATG morphant phenotype but is not sufficient to induce ectopic cnidocytes. Asterisk indicates significant difference from Ctrl MO. Dagger indicates significant difference from SoxB2 ATG MO