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Biology subjects

Rubinstein, H.

Publications and source records attributed to Rubinstein, H..

3 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↗

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↗

Different salicylic and jasmonic acids imbalances are involved in the oxidative stress-mediated cell death, induced by fumonisin B1 in maize seedlings with contrasting resistance to Fusarium verticillioides ear rot in the field.

Background and aimFungal and plant secondary metabolites modulate the plant-pathogen interactions. However, the participation of fumonisins in the Fusarium verticillioides-maize pathosystem is unclear. In this work was studied the cell death, and the reactive oxygen species (ROS) - phytohormone imbalance interplay underlying the phytotoxicity of fumonisin B1 (FB1) in maize germplasms with contrasting resistance to Fusarium ear rot in the field. MethodsResistant (RH) and susceptible hybrid (SH) maize seedlings, grown from uninoculated seeds irrigated with FB1 (1 and 20 ppm), were harvested at 7, 14 and 21 days after planting, and were examined for electrolyte leakage (aerial parts); and for oxidative stress biomarkers (aerial parts and roots). The phytohormone (salicylic and jasmonic acids) imbalance interplay underlying the FB1-induced cell death were further explored in seedlings exposed 24 h to the mycotoxin (1 ppm) in hydroponics. ResultsCell death increased in RH and SH watered with 1 and 20 ppm of mycotoxin, respectively. Both toxin concentrations were pro-oxidant, and the major perturbations were found in roots. An Integrated Biomarker Response index was calculated suggesting that phytotoxicity occurs in a redox context more efficiently controlled by RH. ConclusionThe pre-treatment with the antioxidant ascorbic acid led to the conclusion that cell death in RH was related to a salicylic acid increase mediated by ROS. Nevertheless, FB1 induced two different phytohormonal regulatory mechanisms mediated by oxidative stress in both maize hybrids.

plant biology↗