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Disruption of mRad50 Causes Embryonic Stem Cell Lethality, Abnormal Embryonic Development, and Sensitivity to Ionizing Radiation

Guangbin Luo, Michelle S. Yao, Carla F. Bender, Michael Mills, Anthony R. Bladl, Allan Bradley and John H. J. Petrini
Proceedings of the National Academy of Sciences of the United States of America
Vol. 96, No. 13 (Jun. 22, 1999), pp. 7376-7381
Stable URL: http://www.jstor.org/stable/48066
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Disruption of mRad50 Causes Embryonic Stem Cell Lethality, Abnormal Embryonic Development, and Sensitivity to Ionizing Radiation
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Abstract

The Mre11/Rad50 protein complex functions in diverse aspects of the cellular response to double-strand breaks (DSBs), including the detection of DNA damage, the activation of cell cycle checkpoints, and DSB repair. Whereas genetic analyses in Saccharomyces cerevisiae have provided insight regarding DSB repair functions of this highly conserved complex, the implication of the human complex in Nijmegen breakage syndrome reveals its role in cell cycle checkpoint functions. We established mRad50 mutant mice to examine the role of the mammalian Mre11/Rad50 protein complex in the DNA damage response. Early embryonic cells deficient in mRad50 are hypersensitive to ionizing radiation, consistent with a role for this complex in the repair of ionizing radiation-induced DSBs. However, the null mrad50 mutation is lethal in cultured embryonic stem cells and in early developing embryos, indicating that the mammalian Mre11/Rad50 protein complex mediates functions in normally growing cells that are essential for viability.

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