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The plasma membrane of a cell is subject to stresses causing ruptures that must be repaired immediately to preserve membrane integrity and ensure cell survival. Yet, the spatio‐temporal membrane dynamics at the wound site and the source of the membrane required for wound repair are poorly understood. Here, it is shown that early endosomes, previously only known to function in the uptake of extracellular material and its endocytic transport, are involved in plasma membrane repair in human endothelial cells. Using live‐cell imaging and correlative light and electron microscopy, it is demonstrated that membrane injury triggers a previously unknown exocytosis of early endosomes that is induced by Ca2+ entering through the wound. This exocytosis is restricted to the vicinity of the wound site and mediated by the endosomal soluble N‐ethylmaleimide sensitive factor attachment protein receptor (SNARE) VAMP2, which is crucial for efficient membrane repair. Thus, the newly identified Ca2+‐evoked and localized exocytosis of early endosomes supplies the membrane material required for rapid resealing of a damaged plasma membrane, thereby providing the first line of defense against damage in mechanically challenged endothelial cells. [ABSTRACT FROM AUTHOR]

During implantation, the murine embryo transitions from a "quiet" into an active metabolic/proliferative state, which kick‐starts the growth and morphogenesis of the post‐implantation conceptus. Such transition is also required for embryonic stem cells to be established from mouse blastocysts, but the factors regulating this process are poorly understood. Here, we show that Ronin plays a critical role in the process by enabling active energy production, and the loss of Ronin results in the establishment of a reversible quiescent state in which naïve pluripotency is promoted. In addition, Ronin fine‐tunes the expression of genes that encode ribosomal proteins and is required for proper tissue‐scale organisation of the pluripotent lineage during the transition from blastocyst to egg cylinder stage. Thus, Ronin function is essential for governing the metabolic capacity so that it can support the pluripotent lineage's high‐energy demands for cell proliferation and morphogenesis. Synopsis: Ronin enables active energy production, which is required for the transition from metabolically "quiet" (pre‐implantation) or "quiescent" (diapause) states into a proliferative (post‐implantation) state of embryo development. The metabolic state of the early embryo switches from a "quiet" into an active (proliferative) phase during implantation. Such transition is also required for the establishment of ES cells from mouse blastocysts.Ronin function is essential for proper mitochondrial cristae formation and function, as well as for fine‐tuning the expression of genes that encode ribosomal proteins.In vitro, loss of Ronin results in the establishment of a reversible quiescent state in ES cells, where naïve pluripotency is promoted.In vivo, Ronin governs the metabolic capacity of the embryo for the rapid growth and morphogenesis following implantation. [ABSTRACT FROM AUTHOR]