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Stelzer, Y.

Publications and source records attributed to Stelzer, Y..

7 recordsLinked to original sources

Vascular specification from diversified mesoderm culminates in endothelial convergence

Vasculogenesis establishes the embryonic circulatory system, yet how a common vascular program emerges across multiple embryonic and extraembryonic developmental environments remains incompletely understood. Here, we reconstruct mouse vasculogenesis through integrated single-cell, spatial, lineage and perturbation analyses. We find that vascular specification emerges from distinct sources of pre-specified mesoderm through a transient Kdr+Etv2- vascular-primed state promoted by BMP signaling. Primed cells persist until E8.0- E8.5, after which they resolve into committed derivatives. Dual blood-endothelial potential is largely restricted to early vitelline progenitors, whereas embryonic and umbilical progenitors contribute predominantly to endothelial lineages. Temporal VEGF signaling perturbations validate the inferred specification sequence, placing VEGF downstream of vascular priming and demonstrating its indispensable role in vascular and primitive blood specification. Unlike most developmental lineages, endothelial derivatives converge toward a common transcriptional state while retaining transcriptional traces of their developmental origins. Together, these findings establish a mechanistically validated developmental sequence for mammalian vasculogenesis.

developmental biology↗

A weak-interaction model defines the cell-autonomous function of DNA methylation in gastrulation

DNA methylation is essential for mammalian embryonic development, yet its functional implications remain debated. Here, we introduce a quantitative model that reconciles conflicting perspectives on the roles of methylation in genome regulation and cell specification. Using single-cell multiome analysis in chimeric and whole embryo mutants during mouse gastrulation and organogenesis, we separate cell-autonomous from indirect effects of methylation and demethylation machinery. We show that while the transcriptional and chromatin programs defining basic lineages can be established independently of methylation, the fidelity of differentiated states is severely impaired in its absence. Specifically, we identify hundreds of genes and thousands of cis-regulatory elements (CREs) dependent on methylation for precise regulation. CRE accessibility alterations in methylation mutants are linked with CpG dinucleotide content, and correlate with multiple transcription factor binding motifs. Our data support a weak-interaction model in which DNA methylation moderates, but does not block or instruct the potency of trans-acting regulatory machineries genome-wide.

genomics↗

Histone exchange sensors reveal variant specific dynamics in mouse embryonic stem cells

Eviction of histones from nucleosomes and their exchange with newly synthesized or alternative variants is a central epigenetic determinant. Here, we define the genome-wide incorporation and exchange pattern of canonical and non-canonical histone variants in mouse embryonic stem cells by implementing a recently established, genetically encoded exchange sensor. While exchange of all measured variants scales with transcription, we describe variant-specific associations with transcription elongation and Polycomb binding. We found considerable exchange of H3.1 and H2B variants in heterochromatin and repeat elements, contrasting the stable incorporation and little exchange of H3.3 in these regions. This unexpected association between H3.3 incorporation and exchange of canonical variants is also evident in active promoters and enhancers, and further validated by reduced H3.1 dynamics following depletion of the HIRA H3.3-specific chaperone. The sensor system provides a powerful tool for studying regulation of histone dynamics toward understanding its role in shaping the epigenetic landscape in vivo.

genomics↗

Time-Aligned Hourglass Gastrulation Models in Rabbit and Mouse

The hourglass model describes the convergence of species within the same phylum to a similar body plan during development, yet the molecular mechanisms underlying this phenomenon in mammals remain poorly described. Here, we compare rabbit and mouse time-resolved differentiation trajectories to revisit this model at single cell resolution. We modeled gastrulation dynamics using hundreds of embryos sampled between gestation days 6.0-8.5, and compare the species using a new framework for time-resolved single-cell differentiation-flows analysis. We find convergence toward similar cell state compositions at E7.5, underlied by quantitatively conserved expression of 76 transcription factors, despite divergence in surrounding trophoblast and hypoblast signaling. However, we observed noticeable changes in specification timing of some lineages, and divergence of primordial germ cells programs, which in the rabbit do not activate mesoderm genes. Comparative analysis of temporal differentiation models provides a new basis for studying the evolution of gastrulation dynamics across mammals.

evolutionary biology↗

Mouse-embryo model derived exclusively from embryonic stem cells undergo neurulation and heart development

Several in vitro models have been developed to recapitulate mouse embryogenesis solely from embryonic stem cells (ESCs). Despite mimicking many aspects of early development, they fail to capture the interactions between embryonic and extraembryonic tissues. To overcome this difficulty, we have developed a mouse ESC-based in vitro model that reconstitutes the pluripotent ESC lineage and the two extra-embryonic lineages of the post-implantation embryo by transcription factor-mediated induction. This unified model recapitulates developmental events from embryonic day 5.5 to 8.5, including gastrulation, and formation of the anterior-posterior axis, brain, a beating heart structure, and the development of extraembryonic tissues, including yolk sac and chorion. Comparing single-cell RNA sequencing from individual structures with time-matched natural embryos identified remarkably similar transcriptional programs across lineages, but also showed when and where the model diverges from the natural program. Our findings demonstrate an extra-ordinary plasticity of ESCs to self-organize and generate a whole embryo-like structure.

developmental biology↗

Human primed and naive PSCs are both competent indifferentiating into bona fide trophoblast stem cells

Cells of the trophoblast lineage constitute the major part of placental tissues in higher mammals. Recent derivation of human trophoblast stem cells (TSC) from placental cytotrophoblasts (CT) and from human naive PSCs opens new opportunities for studying development and function of human placenta. Several recent reports have suggested that naive human PSCs retain an exclusive potential to give rise to bona fide TSCs. Here we report that inhibition of TGF{beta} pathway and avoiding WNT stimulation, leads to direct and robust conversion of primed human pluripotent stem cells into TSCs. Systematic side by side comparative analysis showed that the latter are equivalent to previously derived TSC lines. Primed PSC derived TSC lines exhibit self-renewal, are able to differentiate into the main trophoblast lineages, and present RNA and epigenetic profiles that are indistinguishable from the TSC lines derived from placenta or naive PSCs. Our findings underscore a residual plasticity in primed human PSCs that allows converting directly into pre-implantation extra-embryonic cell lineages. HighlightsO_LIPrimed human PSCs readily convert into TSCs upon inhibition of TGF pathway C_LIO_LICHIR inhibits conversion to TSC in primed but not in naive hPSCs C_LIO_LIPrimed human PSC derived TSCs line are indistinguishable from placental and naive derived TSCs C_LIO_LIYAP is sufficient for TSC induction from hPSCs and necessary for TSC maintenance. C_LI

developmental biology↗

High-Resolution Dissection of Conducive Reprogramming Trajectory to Ground State Pluripotency

The ability to reprogram somatic cells into induced pluripotent stem cells (iPSCs) with four transcription factors Oct4, Sox2, Klf4 and cMyc (abbreviated as OSKM)1 has provoked interest to define the molecular characteristics of this process2-7. Despite important progress, the dynamics of epigenetic reprogramming at high resolution in correctly reprogrammed iPSCs and throughout the entire process remain largely undefined. This gap in understanding results from the inefficiency of conventional reprogramming methods coupled with the difficulty of prospectively isolating the rare cells that eventually correctly reprogram into iPSCs. Here we characterize cell fate conversion from fibroblast to iPSC using a highly efficient deterministic murine reprogramming system engineered through optimized inhibition of Gatad2a-Mbd3/NuRD repressive sub-complex. This comprehensive characterization provides single-day resolution of dynamic changes in levels of gene expression, chromatin modifications, TF binding, DNA accessibility and DNA methylation. The integrative analysis identified two transcriptional modules that dominate successful reprogramming. One consists of genes whose transcription is regulated by on/off epigenetic switching of modifications in their promoters (abbreviated as ESPGs), and the second consists of genes with promoters in a constitutively active chromatin state, but a dynamic expression pattern (abbreviated as CAPGs). ESPGs are mainly regulated by OSK, rather than Myc, and are enriched for cell fate determinants and pluripotency factors. CAPGs are predominantly regulated by Myc, and are enriched for cell biosynthetic regulatory functions. We used the ESPG module to study the identity and temporal occurrence of activating and repressing epigenetic switching during reprogramming. Removal of repressive chromatin modifications precedes chromatin opening and binding of RNA polymerase II at enhancers and promoters, and the opposite dynamics occur during repression of enhancers and promoters. Genome wide DNA methylation analysis demonstrated that de novo DNA methylation is not required for highly efficient conducive iPSC reprogramming, and identified a group of super-enhancers targeted by OSK, whose early demethylation marks commitment to a successful reprogramming trajectory also in inefficient conventional reprogramming systems. CAPGs are distinctively regulated by multiple synergystic ways: 1) Myc activity, delivered either endogenously or exogenously, dominates CAPG expression changes and is indispensable for induction of pluripotency in somatic cells; 2) A change in tRNA codon usage which is specific to CAPGs, but not ESPGs, and favors their translation. In summary, our unbiased high-resolution mapping of epigenetic changes on somatic cells that are committed to undergo successful reprogramming reveals interleaved epigenetic and biosynthetic reconfigurations that rapidly commission and propel conducive reprogramming toward naive pluripotency.

developmental biology↗