Organs and tissues have long been known to scale in size with the overall size of the embryo, both as development proceeds and between individuals of different sizes. This is true for somites, segmented structures formed from the presomitic mesoderm (PSM) that give rise to numerous tissues. Somitogenesis is a periodic process driven by a segmentation clock, but how the clock relates to overall somite size is incompletely understood. Now, Kana Ishimatsu, Sean Megason and colleagues investigate somite scaling in zebrafish. Taking into account a delay between somite specification and somite boundary specification, the authors show that somite size scales with PSM size throughout development, both in normal embryos and in size-reduced embryos. Scaling of somite size to PSM size cannot be explained by the period of the segmentation clock, the speed of axis elongation or the travelling wave pattern of segmentation clock genes; in contrast, the Fgf activity gradient does scale with PSM length. The authors construct a ‘clock and scaled gradient’ model to account both for their experimental results and numerous previously published perturbations. Their model makes an additional, unique prediction: ‘echoes’ of somite size changes should follow a brief period of Fgf inhibition, a prediction they corroborate in vivo. Scaling of a molecular gradient thus explains somite scaling during embryogenesis.
