Abstract
Tissue stem cells, such as hematopoietic stem cells (HSCs), have great promise for regenerative medicine. Establishment and maintenance of the hematopoietic system relies on self-renewing HSCs. Genetic studies have identified a number of transcription factors and signaling molecules that control HSC self-renewal, and have delineated the underlying molecular mechanisms. One molecule that has been a particularly useful marker of HSC is Ecotropic viral integration site 1 (Evi1). Evi1 is a transcription factor of the SET/PR domain protein family, and is essential for the maintenance of HSC. Evi1 is notorious for its involvement in leukemia, as Evi1 activation confers the worst prognosis in patients with acute myeloid leukemia. A recent study using Evi1-green fluorescent protein reporter mice demonstrated that in vivo repopulating HSCs are exclusively enriched within the Evi1-expressing fraction in both fetal and adult hematopoietic system. Consistent with predominant expression of Evi1 in HSCs, heterozygous knockout of the Evi1 gene leads to a marked reduction of long-term HSCs with defect of their self-renewal capacity. Here we will summarize the current knowledge regarding the role of Evi1 in hematopoiesis and focus on the specific relationship between Evi1 expression and HSC self-renewal activity.
