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Biology subjects

Schirge, S.

Publications and source records attributed to Schirge, S..

2 recordsLinked to original sources

Endocrine-enriched stem cell-derived islets improve long-term safety in vivo

Fully differentiated stem cell-derived islets (SC-islets) are proven to normalise blood glucose in type 1 diabetic patients. However, the presence of off-target cell types and the immature SC-islet function upon transplantation remain unresolved problems. Here, we established sorting strategies to generate SC-islets with defined glucagon-producing SC-- and insulin-producing {beta}-cell ratios and assessed their safety and efficacy in vitro and in vivo. Engineering SC-islets is beneficial to the insulin response in vitro, which does not translate to improved glycaemic regulation in vivo. Importantly, hormone-producing endocrine cell enrichment and thus off-target cell type depletion eliminated the risk for unwanted outgrowth in vivo. Single cell analysis defined off-target cells in vitro and in vivo and identified marker genes to assess SC-islet quality and define safety release criteria before graft transplantation. This study highlights the importance of determining the SC-islet composition and establishing rigorous quality controls to ensure long-term safety for {beta}-cell replacement therapy.

bioengineering↗

Epiblast morphogenesis is controlled by selective mRNA decay triggered by LIN28A relocation

The embryonic progression from naive to primed pluripotency is accompanied by the rapid decay of pluripotency-associated mRNAs and a concomitant radical morphogenetic sequence of epiblast polarization, rosette formation and lumenogenesis. The mechanisms triggering and linking these events remain poorly understood. Guided by machine learning and metabolic RNA sequencing, we identified RNA binding proteins (RBPs), especially LIN28A, as primary mRNA decay factors. Using mRNA-RBP interactome capture, we revealed a dramatic increase in LIN28A mRNA binding during the naive-rosette-primed pluripotency transition, driven by its nucleolar-to-cytoplasmic translocation. Cytoplasmic LIN28A binds to 3UTRs of pluripotency-associated mRNAs to directly stimulate their decay and drive lumenogenesis. Accordingly, forced nuclear retention of LIN28A impeded lumenogenesis, impaired gastrulation, and caused an unforeseen embryonic multiplication. Selective mRNA decay, driven by nucleo-cytoplasmic RBP translocation, therefore acts as an intrinsic mechanism linking cell identity switches to the control of embryonic growth and morphogenesis.

developmental biology↗