One important question is that of the initial phase of cells which ingress into the PSM. In the cell-autonomous model, that initial phase must be a complex function of time (the clock and trail model of Kerszberg and Wolpert, 2000, also requires an oscillating initial phase). In the Lunatic fringe secretion model, it may be constant. Since the problem of synchronising newly-ingressed cells with posterior PSM is easier if these cells ingress with an oscillating initial phase (data not shown), simulations presented below were carried out with these cells taking on a fixed initial phase when they ingress.
Oscillations in anterior-most cells were stopped on arrival of an expression wave, with a crude, artificial algorithm (the Lunatic fringe secretion model does not seek to address the mechanism by which cells segment). Cells which had segmented were considered not to influence other cells any more, and their oscillatory phase was blocked.
One important aspect of somitogenesis clock oscillations is that the posterior half of the PSM should keep oscillating in near-synchrony (and that the region of synchrony should not extend anteriorly, beyond the middle of the PSM). To reproduce this, it had to be assumed that coupling was stronger in the posterior half of the PSM. This could be an indirect effect of different cell densities in the anterior and posterior halves of the PSM. Alternatively, it could be that FGF8 has the effect of making coupling stronger (FGF8 has been shown to be expressed much more intensely in posterior PSM than in caudal PSM, Dubrulle et al., 2001); this would also explain why the caudal-like domain of clock-gene expression can be extended anteriorly by grafts of FGF8 beads, as shown in Figure 4L by Dubrulle et al. (2001). Stronger coupling in posterior PSM could explain why this region is labile with respect to its segmentation programme, while anterior PSM is not. The effects of FGF8-beads grafts could also be explained by effects on the coupling strength, which will be addressed in a later study.
Simulations were performed with coupling being three times stronger in the caudal PSM than in the rostral PSM, the coupling strength being a continuous but sharp function of the relative position in the PSM (see Appendix A for details). The coupling strength needs not be a continuous function, but this was deemed more biologically realistic.