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Unveiling the mechanisms through which the somitogenesis regulatory networkexerts spatiotemporal control of the somitic patterning has required acombination of experimental and mathematical modeling strategies. Significantprogress has been made for the zebrafish clockwork. However, due to itscomplexity, the clockwork of the amniote segmentation regulatory network hasnot been fully elucidated. Here, we address the question of how oscillationsare arrested in the amniote segmentation clock. We do this by constructing aminimal model of the regulatory network, which privileges architecturalinformation over molecular details. With a suitable choice of parameters, ourmodel is able to reproduce the oscillatory behavior of the Wnt, Notch and FGFsignaling pathways in presomitic mesoderm (PSM) cells. By introducingpositional information via a single Wnt3a gradient, we show that oscillationsare arrested following an infinite-period bifurcation. Notably: theoscillations increase their amplitude as cells approach the anterior PSM andremain in an upregulated state when arrested; the transition from theoscillatory regime to the upregulated state exhibits hysteresis; and anopposing distribution of the Fgf8 and RA gradients in the PSM arises naturallyin our simulations. We hypothesize that the interaction between a limit cycle(originated by the Notch delayed-negative feedback loop) and a bistable switch(originated by the Wnt-Notch positive cross-regulation) is responsible for theobserved segmentation patterning. Our results agree with previously unexplainedexperimental observations and suggest a simple plausible mechanism forspatiotemporal control of somitogenesis in amniotes.

An analysis of overall network architecture reveals an infinite-period bifurcation underlying oscillation arrest in the segmentation clock