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Analyses of human stem cells with distinct GATA6 mutations revealed a spectrum of molecular responses that drive isolated congenital heart disease or the co-occurrence of pancreas and diaphragm malformations.

Single-cell screens during human cardiomyocyte (CM) differentiation reveal that perturbation of congenital heart defect-linked enhancers/genes causes deficient CM differentiation.

Multipotent cardiac precursors within a population of mesoderm are rapidly fated to specific anatomic locations in the developing mouse heart.

Identification of a novel source of progenitor cells that form arterial valve leaflets and that, when disrupted, can lead to bicuspid arterial valve, the most common human cardiac malformation.

An induced pluripotent stem-cell-based, human heart and lung co-differentiation model reveals their shared signaling requirement and enables investigation of their developmental mutual interaction and tissue boundary formation.

Conditional deletion of TGFβ signaling results in tenocyte dedifferentiation in vivo demonstrating a key role for TGFβ signaling in the maintenance of the tendon cell fate.

The transcription factor Nr2f1a represses ventricular and pacemaker cardiomyocyte identities within distinct regions of the zebrafish atrium.

The signaling requirements to decouple proliferation of pancreatic progenitors from differentiation were elucidated and employed for the reproducible expansion, under GMP-compliant conditions, of pancreatic progenitors derived from different human pluripotent stem cell lines.

Sox2 transcription is not correlated with spatial proximity of its essential regulatory enhancer in embryonic stem cells, suggesting gene transcription is not limited to periods of direct enhancer-promoter contact.