Model for involvement of XKLC and GBP in translocation of dorsal determinants. At the onset of cortical rotation (A), KLC bound to KHC on the subcortical microtubule array nucleates particles that include GBP and its binding partner Dsh. As cortical rotation progresses (B), kinesin transports these particles along the rapidly aligning microtubule bundles towards their plus ends, which are oriented toward the prospective dorsal marginal zone (d). Upon reaching the prospective dorsal region (C), Dsh recruits GBP to the ß-catenin degradation complex by binding to Axin (horizontal yellow oblong), which is bound to APC (vertical mauve oblong). GBP dissociates from KLC in favor of binding to GSK3, thereby removing GSK3 from the Axin complex by competing with Axin for its binding. The removal of GSK3 from the degradation complex allows ß-catenin to accumulate in the dorsal region, where it later activates the transcription of dorsal organizer genes.

See Weaver et al., Development 130, 5425-5436 (2003)

Effect of the FGFR inhibitor SU5402 on posterior development in wild-type and ace/fgf8 mutant embryos. (A–D and F) Wild-type and (E and G) ace mutant embryos. All embryos are 24–32 h, anterior to the left. Embryos are stained with an antibody to detect myosin, except E–G, which are unstained. (A–D) Increasing the concentration of SU5402 led to a dose-dependent loss in muscle staining, beginning with the tail. Only tail muscle defects were observed at 15 mM, whereas trunk and tail muscle defects were observed at 30 mM. (E–G) Embryos from obtained from ace/+ adults. (E) Untreated ace mutant embryo, showing typically good posterior development. (F) Wild-type embryo from ace/+ parents treated with 5 mM Su5402; (G) ace mutant embryo treated with 5 mM SU5402 showing severe posterior defects.
 

See Griffin and Kimelman, Developmental Biology  264(2), 456-466 (2003)

Dynamic growth of secondary tails. Confocal microscopic examination of live truncated Bmp receptor-GFP/tbx6-gfp transgenic embryos during secondary tail growth. (A) Time points were started at the 25-somite stage, then taken every hour afterwards, corresponding to approximately one somite per time point at room temperature. Note the growth of the GFP-expressing secondary tail and the maturation of the secondary tail's presomitic mesoderm into somitic blocks. Arrows indicate the second tail, which grows along the primary axis. The asterisk indicates the first fully formed ectopic tail somite at the 25-somite stage.

See Pyati et al., Development 132, 2333-2343 (2005)

Regulation of ptbx6-1.7-gfp and endogenous tbx6 by Wnt and Bmp. (A-J) Lateral views with the animal pole to the top. (A-D) Overexpression of Wnt8. (A,B) Expression of endogenous tbx6 in an uninjected embryo (A) and in an embryo injected with 75 pg of wnt8 RNA (B). The injected embryo shows ectopic expression of tbx6. (C,D) Bright field (C) and fluorescence (D) pictures of a zebrafish embryo coinjected with ptbx6-1.7-gfp and 75 pg of wnt8 RNA showing ectopic GFP fluorescence in the animal pole. (E-H) Expression of endogenous tbx6 in an uninjected embryo (E) and in an embryo injected with 150 pg of Xbmp4 RNA (F). The injected embryo shows ectopic expression of tbx6. (G,H) Bright field (G) and fluorescence (H) pictures of a zebrafish embryo coinjected with ptbx6-1.7-gfp and 150 pg of Xbmp4 RNA at the shield stage showing ectopic GFP fluorescence in the animal pole. (I,J) Bright field (I) and fluorescence (J) pictures of a zebrafish embryo coinjected with ptbx6-1.7-gfp and 25 pg of TVGR RNA showing ectopic GFP fluorescence in the animal pole. TVGR is a constitutively active form of the Tcf transcription factor (Darken and Wilson, 2001). The in situ hybridizations are at shield stage whereas the bright field and fluorescence images are at 50% epiboly.

See Szeto and Kimelman, Development 131, 3751-3760 (2004)