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. 2024 Nov 4;30:196. doi: 10.1186/s10020-024-00965-x

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — m6A modifications in fetal hematopoiesis and HSC maintenance. A Mammalian HSCs are first formed in the aorta-gonad-mesonephros (AGM) region from hemogenic endothelial cells (HECs) as a result of the trans-differentiation process of endothelial-to-hematopoietic transition (EHT). Due to interactions with different readers, m6A-modified transcripts contribute to EHT by promoting pro-EHT, meanwhile suppressing anti-EHT programs. B Nascent fetal HSCs migrate to the fetal liver, undergoing rapid and drastic proliferation. (C) Adult HSCs are maintained in the niche microenvironment of the bone marrow. The schematics of the principal m6A-regulated pathways occurring at these sites are shown in the bottom panel