Abstract
Somite segmentation depends on a gene expression oscillator or clock in the posterior presomitic mesoderm (PSM) and on read-out machinery in the anterior PSM to convert the pattern of clock phases into a somite pattern. Notch pathway mutations disrupt somitogenesis, and previous studies have suggested that Notch signalling is required both for the oscillations and for the read-out mechanism. By blocking or overactivating the Notch pathway abruptly at different times, we show that Notch signalling has no essential function in the anterior PSM and is required only in the posterior PSM, where it keeps the oscillations of neighbouring cells synchronized. Using a GFP reporter for the oscillator gene her1, we measure the influence of Notch signalling on her1 expression and show by mathematical modelling that this is sufficient for synchronization. Our model, in which intracellular oscillations are generated by delayed autoinhibition of her1 and her7 and synchronized by Notch signalling, explains the observations fully, showing that there are no grounds to invoke any additional role for the Notch pathway in the patterning of somite boundaries in zebrafish.
Highlights
The segments of the vertebrate trunk and tail originate from a series of blocks of tissue, the somites, that are formed on each side of the body axis during early development
By mathematical modelling, backed up with measurements on transgenic embryos, we show how Notch signalling may act at a molecular level to synchronise the intracellular oscillators of adjacent individual cells
If Notch signalling is required in the anterior part of the presomitic mesoderm (PSM), the effect on somite segmentation in either case should be more or less immediate, because the somite to form consists of cells exiting from the anterior PSM
Summary
The segments of the vertebrate trunk and tail originate from a series of blocks of tissue, the somites, that are formed on each side of the body axis during early development. Mutations in the Notch cell-cell signalling pathway disrupt somite formation and lead to an irregularly segmented body axis [1,2,3,4,5,6,7,8,9,10,11,12,13,14]. The segmentation clock runs at its full speed in the cells in the posterior part of the PSM, and this dictates the periodicity of the whole process of somite formation: the set of cells emerging from the PSM in the course of one such clock cycle constitute precisely one somite
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