High impact information on Mesp2

• Therefore, 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 [1].
• We isolated a novel bHLH protein gene Mesp2 (for mesoderm posterior 2) that cross-hybridizes with Mesp1 expressed in the early mouse mesoderm [2].
• Mesp2 is expressed in the rostral presomitic mesoderm, but down-regulated immediately after the formation of the segmented somites [2].
• The homozygous Mesp2 (-/-) mice died shortly after birth and had fused vertebral columns and dorsal root ganglia, with impaired sclerotomal polarity [2].
• Tbx6-mediated Notch signaling controls somite-specific Mesp2 expression [3].

Biological context of Mesp2

• In the rostral presomitic mesoderm, rapid downregulation of the Mesp2 expression in the presumptive caudal half somite depends on Ps1 and is a prerequisite for caudal somite half specification [4].
• We conclude from our analyses that Mesp2 functions as a central mediator of such Notch pathways and regulates the gene expression required for rostrocaudal patterning of somites [5].
• Unexpectedly, Ripply2-null embryos show a rostralized phenotype, in contrast to Mesp2-null mice [6].
• Inactivation of the Mesp1 gene results in abnormal heart morphogenesis due to defective migration of heart precursor cells, but somitogenesis is not disrupted because of normal expression of the Mesp2 gene [7].
• In our current report, we identify the essential enhancer element of medaka mesp-b, an orthologue of mouse Mesp2, using transgenic techniques and embryo manipulation [8].

Anatomical context of Mesp2

• Mesp2: a novel mouse gene expressed in the presegmented mesoderm and essential for segmentation initiation [2].
• A bHLH-type transcription factor, Mesp2, plays an essential role in somite segmentation in mice [9].

Regulatory relationships of Mesp2

• The Mesp2 transcription factor establishes segmental borders by suppressing Notch activity [10].

Other interactions of Mesp2

• The Notch target genes Hes5 and Mesp2 were affected to some degree in all mutant embryos [11].
• We propose that the oscillation of Notch activity is arrested and translated in the wavefront by Mesp2 [10].
• Additionally, our epistatic analysis revealed that Mesp2 affects rostrocaudal properties more directly than Dll1 or Dll3 [5].
• LMO4 expression in somite is repressed in mice mutant for the segment polarity gene Mesp2 and expanded in Splotch mutants [12].
• Our study demonstrates that a Ripply2-Mesp2 negative-feedback loop is essential for the periodic generation of the rostro-caudal polarity within a somite [6].

Analytical, diagnostic and therapeutic context of Mesp2

• To determine the function of MesP2 protein (MesP2) in somitogenesis, we generated Mesp2-deficient mice by gene targeting [2].

References