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  Formation of higher-order nuclear Rad51 structures is functionally linked to p21 expression and protection from DNA damage-induced apoptosis

Raderschall, E., Bazarov, A., Cao, J., Lurz, R., Smith, A., Mann, W., et al. (2002). Formation of higher-order nuclear Rad51 structures is functionally linked to p21 expression and protection from DNA damage-induced apoptosis. Journal of Cell Science, 115(1), 153-164.

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 Creators:
Raderschall, Elke1, Author
Bazarov, Alex, Author
Cao, Jiangping, Author
Lurz, Rudi1, Author
Smith, Avril1, Author
Mann, Wolfgang1, Author
Ropers, Hans Hilger2, Author              
Sedivy, John M., Author
Golub, Efim I., Author
Fritz, Eberhard, Author
Haaf, Thomas2, Author              
Affiliations:
1Max Planck Society, ou_persistent13              
2Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433549              

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Free keywords: Apoptosis, Cell cycle arrest, DNA repair, p21, Rad51
 Abstract: After exposure of mammalian cells to DNA damage, the endogenous Rad51 recombination protein is concentrated in multiple discrete foci, which are thought to represent nuclear domains for recombinational DNA repair. Overexpressed Rad51 protein forms foci and higher-order nuclear structures, even in the absence of DNA damage, in cells that do not undergo DNA replication synthesis. This correlates with increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21. Following DNA damage, constitutively Rad51-overexpressing cells show reduced numbers of DNA breaks and chromatid-type chromosome aberrations and a greater resistance to apoptosis. In contrast, Rad51 antisense inhibition reduces p21 protein levels and sensitizes cells to etoposide treatment. Downregulation of p21 inhibits Rad51 foci formation in both normal and Rad51-overexpressing cells. Collectively, our results show that Rad51 expression, Rad51 foci formation and p21 expression are interrelated, suggesting a functional link between mammalian Rad51 protein and p21-mediated cell cycle regulation. This mechanism may contribute to a highly effective recombinational DNA repair in cell cycle-arrested cells and protection against DNA damage-induced apoptosis.

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Language(s): eng - English
 Dates: 2002-01
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: eDoc: 24240
 Degree: -

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Title: Journal of Cell Science
Source Genre: Journal
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Pages: - Volume / Issue: 115 (1) Sequence Number: - Start / End Page: 153 - 164 Identifier: -