A5042394844- Pluripotent Stem Cells Research
- Single-cell and spatial transcriptomics
- Congenital heart defects research
- CRISPR and Genetic Engineering
- RNA Research and Splicing
- Cytokine Signaling Pathways and Interactions
- Tissue Engineering and Regenerative Medicine
University of Nottingham
2022-2024
University of Cambridge
2022
Medical Research Council
2022
Wellcome/MRC Cambridge Stem Cell Institute
2022
University of Padua
2022
Abstract Cell-fate decisions during mammalian gastrulation are poorly understood outside of rodent embryos. The embryonic disc pig embryos mirrors humans, making them a useful proxy for studying gastrulation. Here we present single-cell transcriptomic atlas gastrulation, revealing cell-fate emergence dynamics, as well conserved and divergent gene programs governing early porcine, primate, murine development. We highlight heterochronicity in extraembryonic cell-types, despite the broad...
ABSTRACT We previously demonstrated gradual loss of epiblast during diapause in embryos lacking components the LIF/IL6 receptor. Here, we explore requirement for downstream signalling transducer andactivator transcription STAT3 and its target, TFCP2L1, maintenance naïve pluripotency. Unlike conventional markers, such as NANOG, which remains high until implantation, both TFCP2L1 proteins decline blastocyst expansion, but intensify embryonic region after induction diapause, observed visually...
Abstract Early mammalian gastrulation’s cell-fate decisions are poorly understood due to difficulties obtaining non-rodent embryos. The bilaminar disc of pig embryos mirrors humans, making them a useful proxy for studying gastrulation. Here we present single-cell transcriptomic atlas gastrulation, revealing emergence dynamics, as well conserved and divergent gene programs governing early porcine, primate, murine development. We highlight heterochronicity in extraembryonic cell-type...
Abstract STAT3 has been studied extensively in the context of self-renewal naïve pluripotent mouse embryonic stem cells. We uncovered acute roles for and its target, TFCP2L1, maintenance epiblast primitive endoderm during vivo diapause. On an outbred genetic background, we observed consistent developmental retardation from implantation until day 11.5, beginning with significant reduction cells at Stat3 null embryos. Remarkably, mutants closely resemble non-affected embryos previous all...
Abstract We previously demonstrated gradual loss of epiblast during diapause in embryos lacking components the LIF/IL6 receptor. Here we explore requirement for downstream signalling transducer and activator transcription, STAT3 its target, TFCP2L1, maintenance naïve pluripotency. Unlike conventional markers, such as NANOG, which remains high until implantation, both TFCP2L1 proteins decline blastocyst expansion, but intensify embryonic region after induction diapause, observed visually...