Poly(ADP-ribose) polymerase-1 (Parp-1) localizes mainly in the nucleus and functions in DNA repair, genome stability and cell death regulation. Meanwhile, it also localizes in centrosomes and is involved in the regulation of centrosome duplication. An abnormal increase in centrosome numbers is frequently observed in
Parp-1-deficient (
Parp-1-/-) mouse embryonic fibroblasts (MEFs) (Kanai
et al. (2003) Mol. Cell. Biol.
23, 2451-2462). However, there are no studies on whether the centrosome abnormality occurs also in other cell types under
Parp-1 deficiency. In this study, we report that
Parp-1-/- mouse embryonic stem (ES) cell lines did not show an abnormally increased number of centrosomes compared to wild-type ES cells. Recently, poly(ADP-ribose) glycohydrolase (Parg) has also been shown to localize in centrosomes (Ohashi
et al. (2003) Biochem. Biophys. Res. Commun.
307, 915-921). The number of centrosomes of
Parg-deficient (
Parg-/-) ES cells was also analyzed in this study and was found to be stable under
Parg deficiency. We also examined centrosome numbers in wild-type,
Parp-1-/- and
Parg-/- ES cell lines after treatment with methylmethanesulfonate (MMS) or γ-irradiation. Although a slight increase in the number of centrosomes is observed in each genotype twenty-four hours after treatment with MMS at 50 μM or with γ-irradiation at 1.4 Gy, there was no difference among the genotypes. These results suggest that loss of
Parp-1 and
Parg is insufficient to induce abnormality in centrosome numbers in ES cells and that ES cells possibly possess a strict mechanism for the maintenance of a normal number of centrosomes.
(Contributed by Takashi SUGIMURA, M.J.A.)
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