The tumor suppressor p53 is not required for antigen receptor‐mediated apoptosis of B lymphocytes

Abstract

The tumor suppressor p53 has been shown to be essential in apoptosis induced by irradiation, deregulated c-Myc expression and anti-cancer drugs. The protein level of p53 was moderately increased when the B cell line WEHI-231 undergoes apoptosis by B cell receptor (BCR) crosslinking. However, overexpression of a dominant negative form of p53, p53DD, abolished DNA binding activity of p53 almost completely but failed to block BCR-mediated death of WEHI-231, suggesting that p53-mediated transactivation is not required for BCR-mediated apoptosis of WEHI-231. Moreover, B cells of p53-deficient mice underwent cell death upon BCR crosslinking as efficiently as those of normal littermates, indicating that p53 is not essential for BCR-mediated apoptosis of normal B cells. Although a previous report suggested that p53 is required for BCR-mediated apoptosis through its transactivation, our data strongly argue that p53 is not required for BCR-mediated apoptosis.