| Description: |
The modulation of transcriptional expression of bax, proapoptotic, and bcl-2, antiapoptotic genes, is an early event in the p53 mediated programmed cell death. Oltvai and coworkers related this phenomenon to Bax/Bcl-2 heterodimerization (1). Recently, Knudson et al. proposed the possibility that bax and bcl-2 genes are able to regulate the apoptosis independently (2). Our experimental model, a non-tumorigenic interleukine-3 (IL-3) dependent murine hematopoietic cell line 32D C13(G), which undergoes terminal differentiation into granulocytes when exposed to granulocyte colony stimulating factor (G-CSF), offers a convenient system to study the expression of genes involved in apoptosis. In a previous work, we showed that apoptosis induced by IL-3 deprivation from the culture medium is substained by p53, which in turn modulates the bcl-2 and bax expression (3). In the present work we studied the. heterodimerization of Bax and Bcl-2 by Laser Confocal Microscopy. The IL-3 treated cells showed a low colocalization index of Bax and Bcl-2 (heterodimerization), as detected by immunofluorescence. |