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Colocalization of Sensors Is Sufficient to Activate the DNA Damage Checkpoint in the Absence of Damage
Conclusions: Our results indicate that Rad9 acts as a bona fide signaling adaptor that enables Rad53 phosphorylation by Mec1. Given the high degree of conservation of checkpoint signaling in eukaryotes, we propose that one of the critical functions of checkpoint mediators such as MDC1, 53BP1, or Brca1 is to act as PIKK adaptors during the DNA damage response.
![]() | Rad9 Phosphorylation Sites Couple Rad53 to the Saccharo... Molecular Cell |
![]() Molecular Cell, Volume 9, Issue 5, May 2002, Pages 1055-1065 Marc F. Schwartz, Jimmy K. Duong, Zhaoxia Sun, Jon S. Morrow, Deepti Pradhan, David F. Stern Abstract Rad9 is required for the MEC1/TEL1-dependent activation of Saccharomyces cerevisiae DNA damage checkpoint pathways mediated by Rad53 and Chk1. DNA damage induces Rad9 phosphorylation, and Rad53 specifically associates with phosphorylated Rad9. We report here that multiple Mec1/Tel1 consensus [S/T]Q sites within Rad9 are phosphorylated in response to DNA damage. These Rad9 phosphorylation sites are selectively required for activation of the Rad53 branch of the checkpoint pathway. Consistent with the in vivo function in recruiting Rad53, Rad9 phosphopeptides are bound by Rad53 forkhead-associated (FHA) domains in vitro. These data suggest that functionally independent domains within Rad9 regulate Rad53 and Chk1, and support the model that FHA domain-mediated recognition of Rad9 phosphopeptides couples Rad53 to the DNA damage checkpoint pathway. body.clientWidth*90)/100); var newHeight=document.body.clientHeight; var pdfWin; pdfWin=window.open('','newPdfWin','width='+newWidth+',height='+newHeight+',resizable=yes, left=50, top=50');pdfWin.focus()"> ![]() |
![]() | Telomeres and DNA damage checkpoints Biochimie |
![]() Biochimie, Volume 87, Issue 7, July 2005, Pages 613-624 Valeria Viscardi, Michela Clerici, Hugo Cartagena-Lirola, Maria Pia Longhese Abstract In all eukaryotic organisms, interruptions in duplex DNA molecules elicit a DNA damage response, which includes activation of DNA repair machineries and surveillance mechanisms, known as DNA damage checkpoints. Telomeres and double-strand breaks (DSBs) share the common feature of being physical ends of chromosomes. However, unlike DSBs, telomeres do not activate the DNA damage checkpoints and are usually protected from end-to-end fusions and other processing events that normally promote repair of DNA breaks. This indicates that they are shielded from being recognized and processed as DSBs. On the other hand, chromosome ends resemble damaged DNA, as several factors required for DNA repair and checkpoint networks play important roles in telomere length maintenance. Due to the critical role of both DNA damage checkpoints and telomere homeostasis in maintaining genetic stability and in counteracting cancer development, the knowledge of their interconnections is essential for our understanding of these key cellular controls. ![]() |
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Colocalization of Sensors Is Sufficient to Activate the DNA Damage Checkpoint in the Absence of Damage