This study analyses whether the inability of p53 to induce G 1 arrest after the restriction point relates to an inability to modulate pRb phosphorylation. Transient p53 overexpression in normal human diploid ®broblasts and p53-de®cient cancer cells led to increased levels of the cyclin-dependent kinase inhibitor p21 Cip1/Waf1/Sdi1 and an accumulation of hypophosphorylated pRb in cells growing asynchronously and in cells synchronized in late G 1 or M. Similarly, g-irradiation of asynchronous, late-G 1 , or S phase ®broblasts led to an increase in hypophosphorylated pRb. Experiments with ®broblasts expressing the HPV16 E6 protein indicated that accumulation of hypophosphorylated pRb required functional p53. Progression into and through S phase was not altered by the presence of hypophosphorylated pRb in late G 1 , consistent with the failure of p53 to mediate G 1 arrest in cells that are past the restriction point. These data indicate that accumulation of hypophosphorylated pRb has signi®cantly di erent e ects on cell cycle progression in early G 1 versus late G 1 or S phase.
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