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Science 294 (5547): 1713-1716

Copyright © 2001 by the American Association for the Advancement of Science

ATR and ATRIP: Partners in Checkpoint Signaling

David Cortez,12 Saritha Guntuku,12 Jun Qin,13 Stephen J. Elledge124*

The checkpoint kinases ATM (ataxia telangiectasia mutated) and ATR (ATM and Rad3 related) transduce genomic stress signals to halt cell cycle progression and promote DNA repair. We report the identification of an ATR-interacting protein (ATRIP) that is phosphorylated by ATR, regulates ATR expression, and is an essential component of the DNA damage checkpoint pathway. ATR and ATRIP both localize to intranuclear foci after DNA damage or inhibition of replication. Deletion of ATR mediated by the Cre recombinase caused the loss of ATR and ATRIP expression, loss of DNA damage checkpoint responses, and cell death. Therefore, ATR is essential for the viability of human somatic cells. Small interfering RNA directed against ATRIP caused the loss of both ATRIP and ATR expression and the loss of checkpoint responses to DNA damage. Thus, ATRIP and ATR are mutually dependent partners in cell cycle checkpoint signaling pathways.

1 Verna and Mars McLean Department of Biochemistry and Molecular Biology,
2 Howard Hughes Medical Institute,
3 Department of Cell Biology,
4 Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
*   To whom correspondence should be addressed.

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Human Immunodeficiency Virus Type 1 Vpr Induces DNA Replication Stress In Vitro and In Vivo.
E. S. Zimmerman, M. P. Sherman, J. L. Blackett, J. A. Neidleman, C. Kreis, P. Mundt, S. A. Williams, M. Warmerdam, J. Kahn, F. M. Hecht, et al. (2006)
J. Virol. 80, 10407-10418
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Monoubiquitination of Proliferating Cell Nuclear Antigen Induced by Stalled Replication Requires Uncoupling of DNA Polymerase and Mini-chromosome Maintenance Helicase Activities.
D. J. Chang, P. J. Lupardus, and K. A. Cimprich (2006)
J. Biol. Chem. 281, 32081-32088
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DNA Methyltransferase 1 Knockdown Activates a Replication Stress Checkpoint.
A. Unterberger, S. D. Andrews, I. C. G. Weaver, and M. Szyf (2006)
Mol. Cell. Biol. 26, 7575-7586
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Proteomic Analysis of the Kaposi's Sarcoma-Associated Herpesvirus Terminal Repeat Element Binding Proteins.
H. Si, S. C. Verma, and E. S. Robertson (2006)
J. Virol. 80, 9017-9030
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Chk1- and Claspin-Dependent but ATR/ATM- and Rad17-Independent DNA Replication Checkpoint Response in HeLa Cells..
V. Rodriguez-Bravo, S. Guaita-Esteruelas, R. Florensa, O. Bachs, and N. Agell (2006)
Cancer Res. 66, 8672-8679
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Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection.
D. E. Wilkinson and S. K. Weller (2006)
J. Cell Sci. 119, 2695-2703
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Targeted Deletion of MKK4 in Cancer Cells: A Detrimental Phenotype Manifests as Decreased Experimental Metastasis and Suggests a Counterweight to the Evolution of Tumor-Suppressor Loss.
S. C. Cunningham, E. Gallmeier, T. Hucl, D. A. Dezentje, E. S. Calhoun, G. Falco, K. Abdelmohsen, M. Gorospe, and S. E. Kern (2006)
Cancer Res. 66, 5560-5564
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Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks.
S. Bekker-Jensen, C. Lukas, R. Kitagawa, F. Melander, M. B. Kastan, J. Bartek, and J. Lukas (2006)
J. Cell Biol. 173, 195-206
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