Inducing presomitic mesoderm (PSM)-fated ES cells clarified that Ripply2 directly interacts with Tbx6 and degrades Tbx6 in proteasome-ubiquitin pathway by recruiting the 26S proteasome, which is a PSM-specific event to define the segment border during mouse somitogenesis.

Quantification of fluorescently labeled mRNAs reveals that Fgf4 regulates Notch oscillations in the segmentation clock that controls somitogenesis.

Theory explains how transport of gene expression vortices by cell advection may cause intermingled defective and normal segments along the body axis during resynchronization experiments in the zebrafish segmentation clock.

Cells know when to contribute to the maturing embryonic body axis by adjusting an internal timer to the conditions around them.

Human somites are formed in organoids from human pluripotent stem cells.

Computational modelling together with experimental manipulation indicate that the stability and turnover of activated Notch is inextricably linked to the regulation of the pace of segmentation clock gene expression in the presomitic mesoderm.

In contrast to amniotes, zebrafish (ray-finned fish, teleost) centra are formed from specialised notochord sheath cells, and the segmental patterning of these cells is independent of the segmentation clock.

A noisy cell-intrinsic timer provides positional information for the segmentation clock, modulated by extrinsic factors such as FGF.

Propagation, speed and shapes of genetic waves of expression during development can be modeled by a simple interplay between two transcriptional modules (dynamic/static), which explains robustness and precision of patterning.

Time-lapse recording and theoretical analysis of individual cells isolated from the zebrafish segmentation clock reveal that they behave as self-sustained, autonomous oscillators with distinctive noisy dynamics.