Interaction of human embryonic stem cells (hESC) with human amniotic epithelial cells (hAEC) confers hESC a pluripotent potential that resembles the anteriorized epiblast, which is predisposed to form the neural ectoderm.

Promoter interactome maps in human embryonic stem cells (ESCs) and ESC-derived early neuroectodermal progenitors link distal enhancers to putative target genes, reveal lineage-specific cis-regulatory architecture and shed light on the logic of gene regulation by multiple enhancers.

The transcription machinery used to regulate gene expression and self-renewal in human embryonic stem cells is different from that found in other cells.

Loss and gain-of-function investigation uncovers a regulatory network controlling human heart chamber specification in which the cardiac precursor gene ISL1 accelerates ventricular induction and antagonizes retinoic acid-driven atrial commitment.

Human yolk sac-like cells, which share characteristics with the post-implantation human hypoblast, can model the interaction between the epiblast and hypoblast that occurs during early human development.

Live cell imaging demonstrates that the dynamics of ligand presentation influence signaling through two closely related morphogen signaling pathways in dramatically different ways.

Identifying the pathways that support human naive-state pluripotent stem cells provides insights into the signalling-based regulation of human pluripotency and enables informed decisions to improve conditions for pluripotent cell culture.

Chimeric RNAs are widely distributed spatiotemporally during human retinal development and have important regulatory functions, such as silencing of CTNNBIP1-CLSTN1 biasing the progenitor cells toward the RPE cell fate at the expense of neural retinal cell fates.

Pluripotent stem cell differentiation provides insight into how neural crest subtypes of distinct axial identity are patterned in human embryos.

Analysis of epigenome maps from human pancreatic progenitors and functional validation in zebrafish identify LAMA1 and CRB2 as type 2 diabetes risk-associated genes with roles in pancreatic development.