دورية أكاديمية
أعرض في EDS

The TIP60-ATM axis regulates replication fork stability in BRCA-deficient cells.

التفاصيل البيبلوغرافية
العنوان: The TIP60-ATM axis regulates replication fork stability in BRCA-deficient cells.
المؤلفون: Schleicher EM; Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA., Dhoonmoon A; Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA., Jackson LM; Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA., Khatib JB; Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA., Nicolae CM; Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA., Moldovan GL; Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA. glm29@psu.edu.
المصدر: Oncogenesis [Oncogenesis] 2022 Jun 18; Vol. 11 (1), pp. 33. Date of Electronic Publication: 2022 Jun 18.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: United States NLM ID: 101580004 Publication Model: Electronic Cited Medium: Print ISSN: 2157-9024 (Print) Linking ISSN: 21579024 NLM ISO Abbreviation: Oncogenesis Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: New York, NY : Nature Pub. Group
مستخلص: Maintenance of replication fork stability is essential for genome preservation. Stalled replication forks can be reversed by translocases such as SMARCAL1, and unless protected through the activity of the BRCA pathway, are subsequently subjected to nucleolytic degradation. The ATM and ATR kinases are master regulators of the DNA damage response. ATM activation upon DNA damage is mediated by the acetyltransferase TIP60. Here, we show that the TIP60-ATM pathway promotes replication fork reversal by recruiting SMARCAL1 to stalled forks. This enables fork degradation in BRCA-deficient cells. We also show that this ATM activity is not shared by ATR. Moreover, we performed a series of genome-wide CRISPR knockout genetic screens to identify genetic determinants of the cellular sensitivity to ATM inhibition in wildtype and BRCA2-knockout cells, and validated the top hits from multiple screens. We provide a valuable list of common genes which regulate the response to multiple ATM inhibitors. Importantly, we identify a differential response of wildtype and BRCA2-deficient cells to these inhibitors. In BRCA2-knockout cells, DNA repair genes (including RAD17, MDC1, and USP28) were essential for survival upon ATM inhibitor treatment, which was not the case in wild-type cells. These findings may eventually help guide the way for rational deployment of ATM inhibitors in the clinic.
(© 2022. The Author(s).)
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معلومات مُعتمدة: R01CA244417 U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI); R01 GM134681 United States GM NIGMS NIH HHS; R01 ES026184 United States ES NIEHS NIH HHS; R01ES026184 U.S. Department of Health & Human Services | NIH | National Institute of Environmental Health Sciences (NIEHS); F31 CA243301 United States CA NCI NIH HHS; R01GM134681 U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS); F31CA243301 U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI); R01 CA244417 United States CA NCI NIH HHS
تواريخ الأحداث: Date Created: 20220618 Latest Revision: 20221019
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC9206655
DOI: 10.1038/s41389-022-00410-w
PMID: 35717336
قاعدة البيانات: MEDLINE
الوصف
تدمد:2157-9024
DOI:10.1038/s41389-022-00410-w