Investigating the roles of fetal-specific genes in hematopoiesis

Abstract Hematopoiesis, the process which generates blood cells, changes significantly during mammalian development. Fetal hematopoiesis primarily takes place in fetal liver (FL), where hematopoietic stem cells (FL HSCs) are characterized by high self-renewal capacity and a distinctive program of multilineage differentiation. After birth, main location is bone marrow (BM), (BM less proliferative have more restricted differentiation capacity. How exactly transitions to adult cell-intrinsic properties or environmental factors aid this yet be defined. This project aims elucidate mechanisms behind transition. Studies show that FL BM HSCs distinct gene expression profiles, may account for some their phenotypic differences. Genes, such as LIN28B, encodes an RNA binding protein, highly expressed fetus, absent postnatal life. The re-expression specific genes can confer fetal-like proliferation. Previous work Muljo lab demonstrated LIN28B partially reprograms undergo lymphopoiesis, increased development innate-like lymphocytes. I aim fully reprogram phenotypically resemble ability generate cell types develop early HSCs, though clinically promising, not readily available therapeutic use. Reprogramming suitable alternative could improve current HSC transplantation procedures. supported Intramural Research Program NIAID, NIH. NIAID NIH