Reference Report
| Reference | |||
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| Citation | Kondo, S., Perrimon, N. (2011). A Genome-Wide RNAi Screen Identifies Core Components of the G2-M DNA Damage Checkpoint. Sci. Signal. 4(154): rs1. (Export to RIS) | ||
| FlyBase ID | FBrf0212700 | ||
| Publication Type | Research paper | ||
| PubMed ID | 21205937 | ||
| PubMed Abstract | The DNA damage checkpoint, the first pathway known to be activated in response to DNA damage, is a mechanism by which the cell cycle is temporarily arrested to allow DNA repair. The checkpoint pathway transmits signals from the sites of DNA damage to the cell cycle machinery through the evolutionarily conserved ATM (ataxia telangiectasia mutated) and ATR (ATM- and Rad3-related) kinase cascades. We conducted a genome-wide RNAi (RNA interference) screen in Drosophila cells to identify previously unknown genes and pathways required for the G₂-M checkpoint induced by DNA double-strand breaks (DSBs). Our large-scale analysis provided a systems-level view of the G₂-M checkpoint and revealed the coordinated actions of particular classes of proteins, which include those involved in DNA repair, DNA replication, cell cycle control, chromatin regulation, and RNA processing. Further, from the screen and in vivo analysis, we identified previously unrecognized roles of two DNA damage response genes, mus101 and mus312. Our results suggest that the DNA replication preinitiation complex, which includes MUS101, and the MUS312-containing nuclease complexes, which are important for DSB repair, also function in the G₂-M checkpoint. Our results provide insight into the diverse mechanisms that link DNA damage and the checkpoint signaling pathway. | ||
| DOI | 10.1126/scisignal.2001350 | ||
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| FB2013_03 | |||
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| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
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| Language of Publication | English | ||
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| Publication Type | Journal | ||
| Abbreviation | Sci. Signal. | ||
| Title | Science signaling | ||
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| ISBN/ISSN | 1937-9145 | ||
Data from Reference
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Alleles (20)
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Constructs (8)
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Genes (74)
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Insertions (2)
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Natural transposons (1)
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