A1, a bcl-2 family member, has been identified as a hematopoietic-spec
ific, early inducible gene, In this study it is shown that stable tran
sfection of A1 into an interleukin-3 (IL-3)-dependent myeloid precurso
r cell line, 32D cI3, leads to a retardation of IL-3 withdrawal-induce
d cell death similar to that observed with transfection of bcl-2. Howe
ver, unlike bcl-2 A1 expression permits the accumulation of differenti
ated myeloid cells both before and after IL-3 withdrawal. Total cell a
ccumulation, on the other hand, is considerably greater after IL-3 dep
rivation in the bcl-2 transfectant than in Al-expressing cells. Cells
cotransfected with the two genes behave similarly to cells singly tran
sfected with bcl-2, except that viability following IL-3 withdrawal is
somewhat further enhanced. These results suggest that these two prote
ins have distinct roles that may be related to the divergent regulatio
n of their expression during myeloid differentiation. (C) 1996 by The
American Society of Hematology.