During gastrulation, cardiovascular progenitor cells (CPCs) migrate to the future heart-forming region of the embryo, where they produce the major cardiac lineages. But what regulates CPC fate and behaviour? On , Ian Scott and colleagues report that Smarcd3b (Swi/Snf-related matrix-associated actin-dependent regulator of chromatin subfamily d member 3b) and the transcription factor Gata5 can induce a CPC-like state in zebrafish embryos. In mice, SMARCD3, GATA4 and TBX5 form a cardiac BAF (cBAF) chromatin remodelling complex that promotes myocardial differentiation in the embryonic mesoderm. The researchers now show that smarcd3b and gata5 overexpression in zebrafish embryos leads to the formation of an enlarged heart, whereas combined loss of smarcd3b, gata5 and tbx5 inhibits cardiac differentiation. Most notably, transplantation experiments show that cells overexpressing cBAF components migrate to the developing heart and differentiate into cardiac cells, even if initially placed in non-cardiogenic regions of the embryo. These results show that cBAF has a conserved role in cardiac differentiation and can promote a CPC-like state in vivo.
