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Fanconi anemia genes act to suppress a cross-linker-inducible p53-
independent apoptosis pathway in lymphoblastoid cell lines
FA Kruyt, LM Dijkmans, TK van den Berg and H Joenje
Department of Human Genetics, Free University, Amsterdam, The Netherlands.
Hypersensitivity to cross-linking agents such as mitomycin C (MMC) is
characteristic of cells from patients suffering from the inherited bone
marrow failure syndrome. Fanconi anemia (FA). Here, we link MMC
hypersensitivity of Epstein-Barr virus (EBV)-immortalized FA lymphoblasts
to a high susceptibility for apoptosis and p53 activation. In MMC-treated
FA cells belonging to complementation group C (FA-C), apoptosis followed
cell cycle arrest in the G2 phase. In stably transfected FA-C cells,
plasmid-driven expression of the wild-type cytoplasmic FAC protein relieved
MMC-dependent G2 arrest and suppressed p53 activation. However, in both FA
and non-FA lymphoblasts, p53 seemed not to be instrumental in the induction
of MMC-dependent apoptosis, since overexpression of a dominant-negative p53
mutant failed to affect cell survival. In addition, no differences in the
level of Bcl-2 expression, an inhibitor of apoptosis, were detected between
FA and non- FA cells either in the absence or presence of MMC. Our findings
suggest that FAC and the other putative FA gene products may function in a
yet to be identified p53-independent apoptosis pathway.
Volume 87,
Issue 3,
pp. 938-948,
02/01/1996
Copyright © 1996 by The American Society of Hematology
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