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• W2045791261 abstract "Notch signalling has a key role in the generation of haematopoietic stem cells (HSCs) during vertebrate development; here two adhesion molecules, Jam1a and Jam2a, are shown to be essential for the contact between precursors of HSCs and the somite during embryonic migration, and the Jam1a–Jam2a interaction is shown to be needed to transmit the Notch signal and produce HSCs. Two papers published in this issue of Nature demonstrate the involvement of somites — paired masses of mesoderm cells that form along the anterior–posterior axis of the embryo — in the generation of haematopoietic stem cells (HSCs) during vertebrate development. Phong Dang Nguyen et al. identify a previously unknown somite compartment, called the endotome, which contributes to the formation of the embryonic dorsal aorta by providing endothelial progenitors. The formation of the endotome is regulated by the activity of meox1, a homeobox-containing transcription factor. Isao Kobayashi et al. report that the precursors of HSCs make direct contact with the somite during their embryonic migration and that the interaction is needed to receive the necessary Notch signal. They identify two adhesion molecules that mediate the contact: Jam1a, which is expressed by HSC precursors, and Jam2a, which is expressed by the somite. Notch signalling plays a key role in the generation of haematopoietic stem cells (HSCs) during vertebrate development1,2,3 and requires intimate contact between signal-emitting and signal-receiving cells, although little is known regarding when, where and how these intercellular events occur. We previously reported that the somitic Notch ligands, Dlc and Dld, are essential for HSC specification4. It has remained unclear, however, how these somitic requirements are connected to the later emergence of HSCs from the dorsal aorta. Here we show in zebrafish that Notch signalling establishes HSC fate as their shared vascular precursors migrate across the ventral face of the somite and that junctional adhesion molecules (JAMs) mediate this required Notch signal transduction. HSC precursors express jam1a (also known as f11r) and migrate axially across the ventral somite, where Jam2a and the Notch ligands Dlc and Dld are expressed. Despite no alteration in the expression of Notch ligand or receptor genes, loss of function of jam1a led to loss of Notch signalling and loss of HSCs. Enforced activation of Notch in shared vascular precursors rescued HSCs in jam1a or jam2a deficient embryos. Together, these results indicate that Jam1a–Jam2a interactions facilitate the transduction of requisite Notch signals from the somite to the precursors of HSCs, and that these events occur well before formation of the dorsal aorta." @default.
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• W2045791261 date "2014-08-13" @default.
• W2045791261 modified "2023-09-30" @default.
• W2045791261 title "Jam1a–Jam2a interactions regulate haematopoietic stem cell fate through Notch signalling" @default.
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• W2045791261 doi "https://doi.org/10.1038/nature13623" @default.
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