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Updated: Jun 14, 2026
Three and Four-Dimensional Visualization and Analysis Approaches to Study Vertebrate Axial Elongation and Segmentation
Published on: February 28, 2021
Analysis of Ripply1/2-deficient mouse embryos reveals a mechanism underlying the rostro-caudal patterning within a
Jun Takahashi1, Akiko Ohbayashi, Masayuki Oginuma
1Okazaki Institute for Integrative Biosciences, National Institutes of Natural Sciences, Okazaki, Aichi, Japan.
Abstract:
The rostro-caudal patterning within a somite is periodically established in the presomitic mesoderm (PSM). In the mouse, Mesp2 is required for the rostral property whereas Notch signaling and Ripply2, a Mesp2-induced protein that suppresses Mesp2 transcription, are required for the caudal property. Here, we examined the mechanism behind rostro-caudal patterning by comparing the spatial movement of Notch activity with Mesp2 protein localization in wild-type embryos and those defective in Ripply1 and 2, both of which are expressed in the PSM. Mesp2 protein appears first as a thin band in the middle of the traveling Notch active domain in both wild-type and Ripply1/2-deficient embryos. In wild-type embryos, the Mesp2 band expands anteriorly to the expression front of Tbx6, an activator of Mesp2 transcription. Notch activity becomes localized further anteriorly to this Mesp2 domain, but does not pass over the anterior Mesp2 domain generated in the previous segmentation cycle. As a result, the Notch active domain appears to be restricted between these two Mesp2 domains. In Ripply1/2-deficient embryos, the Mesp2 band becomes more expanded and the Notch domain is finally diminished. Interestingly, Ripply1/2-deficient embryos exhibit anterior expansion of the Tbx6 protein domain, suggesting that Ripply1/2 regulates Mesp2 expression by modulating elimination of Tbx6 proteins. We propose that the rostro-caudal pattern is established by dynamic interaction of Notch activity with two Mesp2 domains, which are defined in successive segmentation cycles by Notch, Tbx6 and Ripply1/2.
Insights
Rostro-caudal patterning in mouse embryos relies on Mesp2 protein and Notch signaling. Ripply1/2 proteins regulate Mesp2 expression by influencing Tbx6 protein levels, establishing precise somite segmentation.
Area of Science:
- Developmental Biology
- Molecular Embryology
- Gene Regulation
Background:
- Somite formation involves rostro-caudal patterning in the presomitic mesoderm (PSM).
- Mesp2 is crucial for rostral patterning, while Notch signaling and Ripply2 govern caudal patterning.
- Ripply1 and Ripply2 are PSM-expressed proteins involved in segmentation.
Purpose of the Study:
- To elucidate the mechanism of rostro-caudal patterning.
- To compare spatial dynamics of Notch activity and Mesp2 protein localization.
- To investigate the roles of Ripply1 and Ripply2 in this process.
Main Methods:
- Analysis of Mesp2 protein localization and Notch activity in wild-type embryos.
- Comparison with embryos deficient in Ripply1 and Ripply2.
- Examination of Tbx6 protein domain expansion in Ripply1/2-deficient embryos.
Main Results:
- Mesp2 protein forms a band within the Notch active domain in both wild-type and mutant embryos.
- In wild-type embryos, Notch activity is restricted between successive Mesp2 domains.
- Ripply1/2 deficiency leads to expanded Mesp2 bands, diminished Notch activity, and anterior Tbx6 expansion.
Conclusions:
- Ripply1/2 regulates Mesp2 expression, potentially by controlling Tbx6 protein elimination.
- Rostro-caudal patterning arises from dynamic interactions between Notch activity and Mesp2 domains.
- This interaction is modulated by Notch, Tbx6, and Ripply1/2 across segmentation cycles.
