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Fig. 2 Her6 is required to repress the proneural gene neurogenin1. In vivo analysis of the loss of Her6 function in double transgenic zebrafish embryos by confocal microscopy. Knock-down of her6 (her6MO) leads to an increase of neurog1 expression in the thalamic complex at 27 hpf (62/86; A and B). At 33 hpf, lack of Her6 function leads to a massive up-regulation of neurog1 in the entire thalamic complex including PTh and MDO (72/91; C and D). The Shh positive MDO is fragmented. Up-regulation of neurog1 leads to a down-regulation of markers, such as dlx4/6:GFP in the PTh at 36 hpf (53/78; E and F). Similarly, the expression of the rTh marker tal1:GFP is completely lacking in her6 morphant embryos 42 hpf (23/28; G and H). By delivering the her6 MO antisense oligomers into a few cells of the rTh by electroporation, neurog1 expression was induced cell-autonomously, as shown by the expression of RFP tagged with a nuclear localisation sequence (5/11; J, higher magnification of the electroporated cell clone marked by arrowheads in J′). Electroporation of a control MO showed no effect (I and I′). III, third brain ventricle; ACeV, anterior cerebral vein; cTh, caudal thalamus; PTh, prethalamus; PTec, pretectum; rTh, rostral thalamus.