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Fig. 7. Involvement of Sox2 as a co-activator in the Fgf response of Xcad3. Structural features of Sox2, its derivatives and SoxD BD(–) examined are illustrated at the bottom. DNA-binding HMG domains and EnR repressor domain are marked. Experimental procedures are as described in Fig. 5 except that the reporter construct (–546/LUC/domain2*) was used in C. (A) Effects of dominant negative Sox2 on the Fgf response of Xcad3/LUC. The injected amounts were 5.3 ( ${blacktriangleup}$ ), 16 ( ${diamondsuit}$ ) or 48 ( ${blacksquare}$ ) pg Sox2-EnR mRNA/blastomere. Sox2-EnR suppresses the Fgf response of the reporter construct (–546/LUC/intron1) in a dose-dependent manner. (B) Effects of wild-type Sox2 on the Fgf response of Xcad3/LUC. The injected amounts were 5.3 ( ${blacktriangleup}$ ), 16 ( ${blacksquare}$ ) or 48 ( ${diamondsuit}$ ) pg Sox2 mRNA/blastomere. (C) Reversal of Sox2-EnR induced suppression of Fgf response by wild-type Sox2. The injected amounts were 16 pg, 96 pg and 112 pg/blastomere for Sox2-EnR, Sox2 and EnR mRNA. Note that the suppression of reporter gene (–546/LUC/domain2*) expression induced by Sox2-EnR ( ${blacktriangleup}$ ) is reversed by the addition of Sox2 ( ${blacksquare}$ ). (D) Effects of Sox2 BD(–) ( ${blacktriangleup}$ ) and SoxD BD(–)( ${blacksquare}$ ) on the Fgf response of Xcad3/LUC. The injected amounts were 160 pg/blastomere for both Sox2 BD(–) and SoxD BD(–) mRNA.

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