Rac2 stimulates Akt activation affecting BAD/Bcl-XL expression while mediating survival and actin function in primary mast cells

Mast cells generated from Rac2-deficient (-/-) mice demonstrated defective actin-based functions, including adhesion, migration, and degranulation. Ra c2(-/-) mast cells generated lower numbers and less mast cell colonies in r esponse to growth factors and were deficient in vivo. Rac2(-/-) mast cells demonstrated a significant reduction in growth factor-induced survival, whi ch correlated with the lack of activation of Akt and significant changes in the expression of the Bcl-2 family members BAD and Bcl-X-L, in spite of a 3-fold induction of Rac1 protein. These results suggest that Rac2 plays a u nique role in multiple cellular functions and describe an essential role fo r Rac2 in growth factor-dependent survival and expression of BAD/Bcl-X-L.