Special Issue Reviews–A Peer Reviewed Forum
Segmental border is defined by the key transcription factor Mesp2, by means of the suppression of notch activity
Article first published online: 29 MAR 2007
Copyright © 2007 Wiley-Liss, Inc.
Special Issue: Special Focus on Segmentation
Volume 236, Issue 6, pages 1450–1455, June 2007
How to Cite
Saga, Y. (2007), Segmental border is defined by the key transcription factor Mesp2, by means of the suppression of notch activity. Dev. Dyn., 236: 1450–1455. doi: 10.1002/dvdy.21143
- Issue published online: 16 MAY 2007
- Article first published online: 29 MAR 2007
- Manuscript Accepted: 26 FEB 2007
- presomitic mesoderm;
- Notch signaling;
- somite patterning;
- segmentation clock
Elaborate somite patterning is based upon dynamic gene regulation within the presomitic mesoderm (PSM), which is derived from the primitive streak and tail bud in the later stage mouse embryo. The Notch signaling pathway and its regulators are major components of most of the events required for temporally and spatially coordinated somite formation. The PSM can be subdivided into at least two domains, based upon transcriptional regulation and gene function. In the posterior PSM, the basic helix–loop–helix (bHLH) protein Hes7 plays a central role in generating a traveling wave of gene expression by negatively regulating the transcription of its target genes. This in turn may define the somite spacing and future segmental units. In the anterior PSM, cells begin to form segmental patterning by acquiring rostral or caudal identities of somite primordia and by defining the segmental border, which must be coupled with the segmentation clock. The link between the clock and segmental border formation is of fundamental importance during somitogenesis. During this process, Mesp2, another basic HLH protein, plays a critical role in the anterior PSM. In this review, I further clarify the dynamic processes leading to segmental border formation in the developing mouse embryo. Developmental Dynamics 236:1450–1455, 2007. © 2007 Wiley-Liss, Inc.