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Human pluripotent stem cell modeling of the ATOH1 lineage identifies a temporal shift in the expression of key transcriptional regulators in the developing human cerebellum, this molecular divergence may drive the protracted development of the human cerebellum compared to rodents.

Loss of YAP1/TAZ expression in the pancreatic endocrine compartment is not a passive consequence of endocrine specification, rather, Hippo pathway-mediated inhibition of YAP1/TAZ in endocrine progenitors is a prerequisite for endocrine specification and differentiation.

Highly reproducible and efficient human primordial germ cell differentiation was achieved through geometric confinement, which enabled quantitative dissection of the cell signaling driving this differentiation, revealing a major role of Wnt signaling is indirect by inducing Nodal signaling.

Quantitative 4D image analysis identifies a group of cells which enter into the otic primordium during morphogenesis and instructs neuronal specification.

Silencing of gene regulatory elements by modifications of DNA-bound proteins promotes the progression of early mouse development.

The dependence of Nematostella germ cell specification on zygotic Hedgehog pathway activity supports the hypothesis that the eumetazoan common ancestor segregated its germline by inductive signals rather than maternal determinants.

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.

A novel regulatory model for the diversification of cardiac cell subpopulations in Drosophila is established by linking epidermal growth factor signaling with differential activities of key transcription factors.

Seastar larvae can regenerate their nervous system by specifying cells to express the gene sox2 to enter neural progenitor states that then follow embryonic gene regulatory modes to form new neurons.

During mouse preimplantation development, the complete loss of actomyosin contractility abolishes cytokinesis but not apico-basal polarisation, lineage specification, or fluid accumulation, which are the critical steps to the formation of the blastocyst.