The heart is first formed in the development of organ, contains four areas (ventricular and atrial), these regions contain perform special functions of cells: the beating heart muscle cells to ensure the pump activity; The vascular cells form the endovascular wall; Pacemaker cell regulates the heartbeat. Unless the heart progenitor cell is produced at the right time, migrated to the right place and differentiated into the right cell type, severe cardiac malformations can occur. In humans, these cardiac malformations are considered congenital heart disease and are the most common cause of severe birth defects in newborns. Previous studies have shown that multiple heart progenitor cells are produced by different cell groups expressing the Mesp1 gene. However, people still don't know how to distinguish between the different at the molecular level of cardiac progenitor cells, and which molecular mechanisms to promote specific heart area or cardiac cell lineage (cardiac lineage).

        In the new study, by the free university of Brussels, stem cells and cancer laboratory Cedric Blanpain professor of the university of Cambridge and Berthold Gottgens professor led a research team using single molecule spectrum (single cell molecular profiling) and lineage tracing (lineage tracking) technology to identify Mesp1 in the earliest stages of cardiovascular cell lineage separation.

         Fabienne Lescroart and colleagues in the different stages of embryonic development express Mesp1 isolated cells, and these early cardiac progenitor cells for single-cell transcriptome analysis, so as to guide and area of cardiac progenitor cells and cell type identity related molecular features. They confirmed that different heart progenitor cells had distinct molecular characteristics.

         To determine the role of transcription factor Mesp1 in regulating the heterogeneity of cardiovascular differentiation procedures and early cardiovascular progenitor cells, They also performed single-cell molecular profiling of these early progenitors in the absence of Mesp1. These experiments show that Mesp1 is required to exit the pluripotent state and activate the cardiovascular gene expression program.