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TRIB2, a serine/threonine pseudokinase identified as an oncogene, is expressed at high levels in the T-cell compartment of hematopoiesis. The proliferation of developing thymocytes is tightly controlled to prevent leukemic transformation of T cells. Here we examine  Trib2  loss in murine hematopoiesis under steady state and proliferative stress conditions, including genotoxic and oncogenic stress.  Trib2   −/−   developing thymocytes show increased proliferation, and  Trib2   −/−   mice have significantly higher thymic cellularity at steady state. During stress hematopoiesis,  Trib2   −/−   developing thymocytes undergo accelerated proliferation and demonstrate hypersensitivity to 5-fluorouracil (5-FU)-induced cell death. Despite the increased cell death post 5-FU-induced proliferative stress,  Trib2   −/−   mice exhibit accelerated thymopoietic recovery post treatment due to increased cell division kinetics of developing thymocytes. The increased proliferation in  Trib2   −/−   thymocytes was exacerbated under oncogenic stress. In an experimental murine T-cell acute lymphoblastic leukemia (T-ALL) model,  Trib2   −/−   mice had reduced latency  in vivo , which associated with impaired MAP kinase (MAPK) activation. High and low expression levels of  Trib2  correlate with immature and mature subtypes of human T-ALL, respectively, and associate with MAPK. Thus, TRIB2 emerges as a novel regulator of thymocyte cellular proliferation, important for the thymopoietic response to genotoxic and oncogenic stress, and possessing tumor suppressor function.

TRIB2 regulates normal and stress-induced thymocyte proliferation