p53 binds single-stranded DNA ends and catalyzes DNA renaturation and strand transfer.

Bakalkin, Georgy; Yakovleva, Tatjana; Selivanova, Galina; Magnússon, Kristinn P.; Szekeres, L.; Киселева, Елена; Klein, George; Terenius, Lars; Wiman, Klas G.

doi:10.1073/pnas.91.1.413

Cited by 260 publications

(152 citation statements)

References 17 publications

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“…These properties led to the suggestion that p53 represses DNA replication by inhibiting the unwinding of the DNA at replication origins. Such a function is also in keeping with the observation that p53 can promote DNA or RNA re-annealing, a reaction which opposes the unwinding (Oberosler et al, 1993;Bakalkin et al, 1994Bakalkin et al, , 1995Brain and Jenkins, 1994. p53 is normally expressed at a very low level (Crawford et al, 1981;Benchimol et al, 1982;May et al, 1991). Most of the results implicating p53 in either transcription or replication were obtained using in vitro systems in which p53 was over-expressed, thus representing non-physiological conditions.…”

Section: Introductionsupporting

confidence: 67%

A functional analysis of p53 during early development of xenopus laevis

et al. 1997

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p53 is a nuclear protein that acts like a tumor suppressor and is involved in regulation of cellular growth. In Xenopus, the p53 protein is highly expressed during oogenesis and is strictly cytoplasmic in the oocyte. We have analysed its participation in DNA replication and transcription during early development, using the egg and oocyte as model-systems. The injection of sperm nuclei into Xenopus eggs is followed by DNA replication and mitotic events. We show that the endogenous p53 enters the nuclei and moves through a series of discrete subnuclear loci whose distribution is S-phase speci®c. A speci®c peripheral nuclear localization of p53 is observed before entry into S-phase, followed by an internal localization which is strictly dependent on ongoing DNA synthesis. At no stage in the cell cycle, however, did we observe any co-localization with RPA or PCNA, which were used as initiation or elongation markers for DNA replication. We also show that injection into the nucleus of the oocyte of small amounts of either Xenopus or human p53 ± less than 10% of the cytoplasmic storage ± is su cient to block RNA polymerase IIdependent transcription from a coinjected TATA-boxcontaining reporter plasmid. Transcription is rescued by microinjection of the TATA-box binding protein (TBP), suggesting that nuclear exclusion of p53 during oogenesis may be necessary for transcription of maternal genes. These characteristics are discussed in relation to the regulation of nuclear activities during early embryogenesis.

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Section: Introductionsupporting

confidence: 67%

A functional analysis of p53 during early development of xenopus laevis

et al. 1997

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“…StuÈ rzbecher et al (1996) mapped the interaction with the Rad51 recombinase, a central homologous pairing and strand exchange protein, to central regions of the p53 protein. The central core domain was found to contain p53's intrinsic exonuclease activity (Mummenbrauer et al, 1996;Janus et al, 1999b) and also binds non-speci®cally to internal regions of single-stranded DNA (Bakalkin et al, 1994). Apparently, the conformational change induced by the amino acid exchange Alanin to Valin at position 135 was not su cient to disrupt the presumptive regulatory domain in our study.…”

Section: How Does P53 Regulate Homologous Recombination?mentioning

confidence: 48%

Dissociation of p53-mediated suppression of homologous recombination from G1/S cell cycle checkpoint control

et al. 2000

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The tumor suppressor p53 is considered as the guardian of the genome which is activated following genotoxic stress. In many cell types, p53 mediates G1 cell cycle arrest as the predominant cellular response. Inactivation of wild-type p53 leads to loss of G1/S checkpoint control and to genomic instability, including increased spontaneous homologous recombination (HR). To determine whether regulation of the G1/S checkpoint is required for suppression of HR, we assessed recombination events using a plasmid substrate that stably integrated into the genome of p53-null mouse ®broblasts. Exogenous expression of a temperature-sensitive p53 protein (Ala135 to Val), which had lost trans-activation function and could not regulate G1/S transition when in mutant conformation, reduced HR rates to the same extent as wild-type p53. Furthermore, a p53 construct with an alternatively-spliced carboxy terminus also retained this ability in the absence of both activities, G1/S control and non-sequence speci®c DNA binding as mediated by the carboxy terminus. Our data dissociate regulation of HR by p53 from its role as a cell cycle checkpoint protein.The results support a model which extends p53's role as a guardian of the genome to include transactivationindependent regulatory functions in DNA repair, replication and recombination. Oncogene (2000) 19, 632 ± 639.

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“…On the basis of their results, the authors suggest that p53 interaction with Rad51 may in¯uence DNA recombination and repair and that additional modi®cations of p53 by mutations and protein binding may a ect this interaction. In addition, p53 has been shown to bind single stranded DNA ends (Bakalkin et al, 1994) and to possess strong DNA-DNA and RNA-RNA strand annealing activity (Bakalkin et al, 1994;Oberosler et al, 1993;Brain and Jenkins, 1994).…”

Section: Other Biochemical Activities Of P53mentioning

confidence: 99%