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The Mesp2 transcription factor establishes segmental borders by suppressing Notch activity
TLDR
Ex vivo levels of Notch1 activity in mice are visualized, showing that it oscillates in the posterior PSM but is arrested in the anterior PSM, and it is proposed that the oscillation of notch activity is arrested and translated in the wavefront by Mesp2.
Mesp2 initiates somite segmentation through the Notch signalling pathway
TLDR
Mesp2- and Ps1-dependent activation of Notch-signalling pathways might differentially regulate Dll1 expression, resulting in the establishment of the rostro-caudal polarity of somites.
TRB3 suppresses adipocyte differentiation by negatively regulating PPARgamma transcriptional activity.
TLDR
Evidence is provided that TRB3 acts as a potent negative regulator of PPARgamma, a master regulator of adipocyte differentiation, and tightly controls adipogenesis.
Tbx6-mediated Notch signaling controls somite-specific Mesp2 expression.
TLDR
The data reveal that a mechanism, via Tbx6-dependent Notch signaling, acts on the transcriptional regulation of Mesp2, and uncovers an additional component of the interacting network of various signaling pathways that are involved in somitogenesis.
The oscillation of Notch activation, but not its boundary, is required for somite border formation and rostral-caudal patterning within a somite
TLDR
A progressive oscillating wave of Notch activity is translated into the rostral-caudal polarity of a somite by regulating Mesp2 expression in the anterior PSM, which indicates that the initial somite pattern can be defined as a direct output of the segmentation clock.
Identification of Epha4 enhancer required for segmental expression and the regulation by Mesp2
TLDR
Transgenic and transient luciferase analyses determined that the presence of repeated E-box sequences is a minimum essential requirement for the expression in the anterior PSM, and showed that Mesp2 directly binds to the enhancer sequence of Epha4.
The orphan nuclear receptor RORalpha restrains adipocyte differentiation through a reduction of C/EBPbeta activity and perilipin gene expression.
TLDR
It is shown that RORalpha inhibits the transcriptional activity of CCAAT/enhancer-binding protein beta without affecting its expression, thereby blocking the induction of both PPARgamma and C/EBPalpha, resulting in the suppression of C/EBPbeta-dependent adipogenesis.
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