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Fig. 6. Lower level reduction of FGF8a and FGF8b or strong reduction of FGF8a alone with XlMOF8, MOSDF8 and MOSAF8a prevents proper formation of posterior neural tissue at the early neurula stage.X. laevis embryos displayed dorsoanteriorly. Pink staining indicates the lineage tracer; embryos injected into one cell at the two- or four-cell stage. (A,E,I,M) Control MO (40 ng); (B,F,J,N) MOF8 20 ng; (C,G,K,O) MOSDF8 43 ng; (D,H,L,P) MOSAF8a 60 ng. (A-D) XlMOF8 (44/45), MOSDF8 (18/19) and MOSAF8a (38/39) cause a mispatterning of sox2 expression. (E-H) otx2 expression is expanded toward the posterior after XlMOF8 (23/25), MOSDF8 (20/20) and MOSAF8a (26/29) injection, while the posterior neural gene dbx is absent (MOF8, 25/25; MOSDF8, 20/20; MOSAF8a, 35/38). (I-L) en2 expression is diminished and sometimes completely absent on the injected side: XlMOF8 (13/13), MOSDF8 (17/17) and MOSAF8a (32/33). (M-P) both the spinal cord domain (hoxB9) and the hindbrain domain (krox20) is strongly reduced and shifted toward the posterior of the embryo on the XlMOF8 (42/42), MOSDF8 (20/20) and MOSAF8a (40/40) injected side of the embryo. Effects on the uninjected side are present but much weaker. (Q-S) Neural tube stage 20 embryos treated as indicated; (T-V) FGF8a mRNA (50 pg) rescued the reduction of hoxB9 caused by XlMOF8 (32/44), MOSAF8a (19/35) and MOSDF8 (19/20). |
