Transcription factor. Plays a role in the epithelialization of somitic mesoderm and in the development of cardiac mesoderm. Defines the rostrocaudal patterning of the somites by participating in distinct Notch pathways. No expression was detected in adult tissues except the testis. Expression in the testis was regulated developmentally; expressed 2 weeks after birth, and increases, reaching the full expression level in mature testes. The earliest expression is detected at the junction of the epiblast and extraembryonic ectoderm, which is the initiation site for gastrulation. Around 6.5-6.75 dpc, expression becomes evident as gastrulation progresses. Expression does not spread over all mesodermal cells; it is seen only in a fraction of cells, particularly those in the early emergence group destined to become the extraembryonic mesoderm and the most posterior part of the tailbud. Expression remains for a while at the base of the allantois, and then spreads out to the lateral margins of the tail bud mesoderm. Expressed in the anterior presomitic mesoderm in a broad or thin stripe pattern. Expressed in the paraxial mesoderm during somitogenesis. Expression disappears before 8.5 dpc. Expression is induced by Notch signaling. Mice embryos exhibit defects in single heart tube formation, due to a delay in mesodermal migration. However, the cells eventually acquired migratory activity and gave rise to an abnormal heart tube. Mice lacking Mesp1 and Mesp2 die around 9.5 dpc. The major defect is the apparent lack of any mesodermal layer between endoderm and ectoderm and a defect in the migratory activity of mesodermal cells. It seems that a compensatory mechanism exists in which Mesp1 expression is up-regulated in the absence of Mesp2. Mesp1 may be involved in the rescue of somitogenesis in the null Mesp2 embryos.