Speaker
Description
In the early embryo an intracellular oscillator known as the segmentation clock patterns the somites, blocks of mesoderm that give rise to vertebrae and skeletal muscle. Clock oscillations are coupled between cells of the pre-somitic mesoderm (PSM) via notch-delta signalling, synchronising differentiation of PSM cells into somites. While this is happening, PSM cells are rearranging and dividing, and are being replaced by new cells that ingress from surrounding tissues. The relative contribution of each of these processes to elongation of the PSM varies across species, facilitating the evolution of diverse body plans and ecological niches.
However, processes like cell ingression and division disrupt synchrony of the clock and could affect somite patterning if these events occur too often. How then does the diversity of morphogenetic dynamics evolve without disrupting the clock, and how does this ‘evolvability’ depend on the clock itself? Using a phase oscillator model to describe clock coupling, and a point-based model to describe cell movement, we studied how clock dynamics react to varying morphogenesis of the PSM. We find that clock dynamics are robust to changing morphogenesis when oscillator coupling is of the correct magnitude and timescale. By experimentally quantifying coupling in Lake Malawi cichlids, we show that these conditions are satisfied across 34% of extant vertebrate species. This suggests that clock coupling has permitted the evolution of diverse body plans.
