Hematopoietic stem cells (HSCs) are responsible for the lifelong production of all blood cells1. Like many other tissues and organs, the hematopoietic system develops during embryogenesis2. One of the challenges of this developing process is to generate a functional HSC pool, which is a prerequisite for seeding bone marrow and thereafter lifelong hematopoiesis3. HSC expansion is critical for the establishment of such HSC pool2. To accomplish the expansion, the fetal liver HSCs (FL-HSCs) are continuously undergoing symmetric cell division, which requires precise collaboration of multiple cellular processes2, especially those that serve to maintain the genomic stability of the dividing HSCs. Many factors have been shown to be involved in FL-HSC expansion. Growth factors such as insulin-like growth factor 2 (IGF2) and stem cell factor (SCF) stimulate FL-HSC proliferation4,5, and key transcription factors such as Gata2 and PU.1 regulate the proliferation and maintenance of fetal HSCs by regulating multiple downstream target genes6,7. However, the intrinsic factors that directly regulate FL-HSC expansion remain to be investigated.

Lis1 is identified as the first lissencephaly gene, and is well-known for its function in regulating the microtubule (MT)-associated proteins8. By interacting with different partners, Lis1 participates in several critical cell functions, including mitosis, actin cytoskeleton regulation and membrane protein trafficking8,9. Notably, Lis1 controls mitotic spindle orientation and MT plus-end dynamics to ensure precise cell division via the Lis1-NDEL1-dynein complex10. Together, the primary function of Lis1 in mammalian cells is to regulate MT-associated processes and facilitate cell division.

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