GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE307nnn/GSE307390/primary200OKTranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE307390GEOGSEfalseIn situ fate mapping identifies the neonatal origin of platelet-biased hematopoietic stem cellsHematopoietic stem cells (HSCs) display heritable and deterministic gene regulatory states associated with functional heterogeneity. However how these biased fate programs change through development remains poorly understood. Here, using single-cell lineage tracing, we map the function and state of thousands of individual mouse HSCs spanning from the earliest mature fetal stages until young adults. We identify a burst of platelet- and myeloid-biased HSCs during the first postnatal week. Fetal HSCs retain a fetal-like program even after 4 months in the recipient bone marrow, suggesting that the adult HSC program is epigenetically configured early after birth. Creating a single-cell atlas of mouse perinatal HSCs, we identify a transient HSC state with hallmarks of Epithelial-Mesenchymal Transition (EMT), mTOR complex 1 activity, and cholesterol synthesis (SREBP targets). Tracing the rare cells that traverse this transient state, we reveal the neonatal origin of long-term platelet/myeloid-biased HSCs in both native and transplantation hematopoiesis. Transient treatment with mTORC1 inhibitor rapamycin during the first postnatal week suffices to reduce the platelet-biased adult HSC programming, without affecting total HSC numbers. In sum, we reveal a late developmental origin for platelet-biased HSCs, with important implications for hematopoietic aging.2026/09/01GSE307390GSM9223254GSM9223243GSM9223265GSM9223255GSM9223244GSM9223263GSM9223252GSM9223253GSM9223264GSM9223242GSM9223250GSM9223261GSM9223251GSM9223262GSM9223260GSM9223249GSM9223258GSM9223247GSM9223248GSM9223259GSM9223245GSM9223256GSM9223257GSM922324624247307390Mus musculus