FIGURE 5 | Manipulation of an Fgf signal alters somite size in zebrafish.

a | The pattern of MAPK activation (left) closely resembles that of fgf8 expression (right) in 10-somite zebrafish embryos. The embryos were immunostained with an antibody against an activated (di-phosphorylated) form of ERK (a vertebrate MAPK). Lateral views are shown. The strong activation is detected in the posterior two-thirds of the PSM (arrow). The activation domain roughly corresponds to region I. Weak activation is detected in newly formed somites (arrowhead). (Modified from Ref. 42.) b | Schematic representations of the effect of Fgf signalling on somite-border formation. The expression of her1, which is cyclic (grey) in the presence of higher Fgf signalling, becomes stabilized (purple) as Fgf levels decline in region I. The stabilized her1 marks a presumptive future somite border (dashed line). When an Fgf signal is transiently compromised by SU5402, a kinase inhibitor that might be specific to all types of Fgf receptors, waves of her1 expression prematurely terminate in the intermediate PSM instead of in the anterior PSM, due to acceleration of PSM maturation. The posterior shift in her1 termination is accompanied by a posterior shift in the expression of segmentation genes, such as a zebrafish mesp gene⁴². As a result, the point of segment formation moves towards the tailbud, giving rise to a larger somite (left panel). By contrast, an exogenous Fgf signal that is provided by Fgf-soaked beads maintains the PSM in an immature state for a longer period and, therefore, causes anterior expansion of region I. Eventually, her1 expression reaches further to the anterior than it does on the control side, and a somite border forms more anteriorly, resulting in a smaller somite (right panel). (fgf8, fibroblast growth factor 8; her1, hairy-related 1; MAPK, mitogen-activated protein kinase; mesp, mesoderm posterior; PSM, presomitic mesoderm.)

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