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1 Research Institute of Molecular Pathology (IMP), A-1030
Vienna, Austria;
2 International Agency for Research on Cancer
(IARC), F-69008 Lyon, France;
3 Department of Cytology and
Genetics, University of Vienna, A-1030 Vienna, Austria;
4 Department of Molecular Oncology/ Pediatry,
German Cancer Research Center, D-69120 Heidelberg, Germany;
5 Medical Clinics, University of Tübingen,
D-72076 Tübingen, Germany
Mice lacking the gene encoding poly(ADP-ribosyl) transferase (PARP
or ADPRT) display no phenotypic abnormalities, although aged mice are
susceptible to epidermal hyperplasia and obesity in a mixed genetic
background. Whereas embryonic fibroblasts lacking PARP exhibit normal
DNA excision repair, they grow more slowly in vitro. Here we
investigated the putative roles of PARP in cell proliferation, cell
death, radiosensitivity, and DNA recombination, as well as chromosomal
stability. We show that the proliferation deficiency in vitro and in
vivo is most likely caused by a hypersensitive response to
environmental stress. Although PARP is specifically cleaved during
apoptosis, cells lacking this molecule apoptosed normally in response
to treatment with anti-Fas, tumor neurosis factor 
, 
-irradiation,
and dexamethasone, indicating that PARP is dispensable in apoptosis and
that PARP
/ thymocytes are not hypersensitive to
ionizing radiation. Furthermore, the capacity of mutant cells to carry
out immunoglobulin class switching and V(D)J recombination is
normal. Finally, primary PARP mutant fibroblasts and splenocytes
exhibited an elevated frequency of spontaneous sister chromatid
exchanges and elevated micronuclei formation after treatment with
genotoxic agents, establishing an important role for PARP in the
maintenance of genomic integrity.
[Key Words: PARP inactivation; aggregation of embryos; stress response; apoptosis; recombination; sister chromatid exchange]
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