Mesp2: a novel mouse gene expressed in the presegmented mesoderm and essential for segmentation initiation

• Published in: Genes & development Vol. 11; no. 14; pp. 1827 - 1839
• Main Authors: Saga, Y, Hata, N, Koseki, H, Taketo, M M
• Format: Journal Article
• Language: English
• Published: United States 15.07.1997
• Subjects: Amino Acid Sequence; Animals; Base Sequence; Basic Helix-Loop-Helix Transcription Factors; Bone and Bones - abnormalities; Cloning, Molecular; DNA, Complementary; Embryonic and Fetal Development - genetics; Fibroblast Growth Factors - genetics; Gene Expression Regulation, Developmental; Homozygote; Membrane Proteins - genetics; Mesoderm; Mice; Mice, Inbred C57BL; Molecular Sequence Data; Receptors, Notch; Sequence Homology, Amino Acid; Transcription Factors - genetics; Transcription Factors - physiology
• ISSN: 0890-9369; 1549-5477
• DOI: 10.1101/gad.11.14.1827

We isolated a novel bHLH protein gene Mesp2 (for mesoderm posterior 2) that cross-hybridizes with Mesp1 expressed in the early mouse mesoderm. Mesp2 is expressed in the rostral presomitic mesoderm, but down-regulated immediately after the formation of the segmented somites. To determine the function of MesP2 protein (MesP2) in somitogenesis, we generated Mesp2-deficient mice by gene targeting. The homozygous Mesp2 (-/-) mice died shortly after birth and had fused vertebral columns and dorsal root ganglia, with impaired sclerotomal polarity. The earliest defect in the homozygous embryos was a lack of segmented somites. Their disruption of the metameric features, altered expression of Mox-1, Pax-1, and Dll1, and lack of expression of Notch1, Notch2, and FGFR1 suggested that MesP2 controls sclerotomal polarity by regulating the signaling systems mediated by notch-delta and FGF, which are essential for segmentation.