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Background  The polycomb-group (PcG) proteins function as general regulators of stem cells. We previously reported that retrovirus-mediated overexpression of  Bmi1 , a gene encoding a core component of polycomb repressive complex (PRC) 1, maintained self-renewing hematopoietic stem cells (HSCs) during long-term culture. However, the effects of overexpression of  Bmi1  on HSCs  in vivo  remained to be precisely addressed.    Methodology/Principal findings  In this study, we generated a mouse line where  Bmi1  can be conditionally overexpressed under the control of the endogenous  Rosa26  promoter in a hematopoietic cell-specific fashion ( Tie2-Cre;R26Stop FL Bmi1 ). Although overexpression of  Bmi1  did not significantly affect steady state hematopoiesis, it promoted expansion of functional HSCs during  ex vivo  culture and efficiently protected HSCs against loss of self-renewal capacity during serial transplantation. Overexpression of  Bmi1  had no effect on DNA damage response triggered by ionizing radiation. In contrast,  Tie2-Cre;R26Stop FL Bmi1  HSCs under oxidative stress maintained a multipotent state and generally tolerated oxidative stress better than the control. Unexpectedly, overexpression of  Bmi1  had no impact on the level of intracellular reactive oxygen species (ROS).    Conclusions/Significance  Our findings demonstrate that overexpression of  Bmi1  confers resistance to stresses, particularly oxidative stress, onto HSCs. This thereby enhances their regenerative capacity and suggests that Bmi1 is located downstream of ROS signaling and negatively regulated by it.

Bmi1 Confers Resistance to Oxidative Stress on Hematopoietic Stem Cells