An additional form of rat Bcl-x, Bcl-x beta, generated by an unspliced RNA, promotes apoptosis in promyeloid cells

The bcl-2 oncogene product delays apoptotic cell death and prolongs the cell survival, We cloned two bcl-2-related cDNAs from a rat thymus cDNA library by low stringency hybridization with a rat bcl-2 fragment as a probe. One of these, designated bcl-x alpha, was a counterpart of the human bcl-x(L) reported previously as a bcl-2-related gene (Boise, L. H., Gonzalez-Garcia, M., Postema, C. E., Ding, L., Lindsten, T., Turka, L. A., Mao, M., Nunez, G., and Thompson, C. B. (1993) Cell 74, 597-608). The other, designated bcl-x beta, was novel and found to be generated by an unspliced mRNA, whereas bcl-x alpha was generated from a spliced transcript. The splice junction exactly corresponded to that found in the bcl-2 gene. bcl-x beta was specifically expressed in cerebellum, heart, and thymus. When bcl-x beta directed by a strong promoter was introduced into an interleukin-3-dependent promyeloid cell line, FDC-P1, DNA fragmentation was observed even in the growing state in the presence of interleukin-3 although not in the control transfectants. This finding suggests that the rat bcl-x beta gene product promotes apoptosis in the promyeloid cells.