Details and Concerns Regarding the G2/M DNA Damage Checkpoint in Budding Yeast

2000 ◽  
Vol 65 (0) ◽  
pp. 433-442 ◽  
Author(s):  
T. WEINERT ◽  
E. LITTLE ◽  
L. SHANKS ◽  
A. ADMIRE ◽  
R. GARDNER ◽  
...  
2003 ◽  
pp. 197-202
Author(s):  
Marco Muzi-Falconi ◽  
Michele Giannattasio ◽  
Giordano Liberi ◽  
Achille Pelliccioli ◽  
Paolo Plevani ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e65875 ◽  
Author(s):  
Bilge Argunhan ◽  
Sarah Farmer ◽  
Wing-Kit Leung ◽  
Yaroslav Terentyev ◽  
Neil Humphryes ◽  
...  

2008 ◽  
Vol 28 (15) ◽  
pp. 4782-4793 ◽  
Author(s):  
Fabio Puddu ◽  
Magda Granata ◽  
Lisa Di Nola ◽  
Alessia Balestrini ◽  
Gabriele Piergiovanni ◽  
...  

ABSTRACT Following genotoxic insults, eukaryotic cells trigger a signal transduction cascade known as the DNA damage checkpoint response, which involves the loading onto DNA of an apical kinase and several downstream factors. Chromatin modifications play an important role in recruiting checkpoint proteins. In budding yeast, methylated H3-K79 is bound by the checkpoint factor Rad9. Loss of Dot1 prevents H3-K79 methylation, leading to a checkpoint defect in the G1 phase of the cell cycle and to a reduction of checkpoint activation in mitosis, suggesting that another pathway contributes to Rad9 recruitment in M phase. We found that the replication factor Dpb11 is the keystone of this second pathway. dot1Δ dpb11-1 mutant cells are sensitive to UV or Zeocin treatment and cannot activate Rad53 if irradiated in M phase. Our data suggest that Dpb11 is held in proximity to damaged DNA through an interaction with the phosphorylated 9-1-1 complex, leading to Mec1-dependent phosphorylation of Rad9. Dpb11 is also phosphorylated after DNA damage, and this modification is lost in a nonphosphorylatable ddc1-T602A mutant. Finally, we show that, in vivo, Dpb11 cooperates with Dot1 in promoting Rad9 phosphorylation but also contributes to the full activation of Mec1 kinase.


DNA Repair ◽  
2011 ◽  
Vol 10 (11) ◽  
pp. 1086-1094 ◽  
Author(s):  
Carolyn M. George ◽  
Amy M. Lyndaker ◽  
Eric Alani

2000 ◽  
Vol 6 (2) ◽  
pp. 487-492 ◽  
Author(s):  
Janos Demeter ◽  
Sang Eun Lee ◽  
James E. Haber ◽  
Tim Stearns

PLoS ONE ◽  
2017 ◽  
Vol 12 (7) ◽  
pp. e0180556 ◽  
Author(s):  
Li-Ting Diao ◽  
Chin-Chuan Chen ◽  
Briana Dennehey ◽  
Sangita Pal ◽  
Pingping Wang ◽  
...  

Genetics ◽  
2000 ◽  
Vol 155 (4) ◽  
pp. 1577-1591 ◽  
Author(s):  
Maria Pia Longhese ◽  
Vera Paciotti ◽  
Holger Neecke ◽  
Giovanna Lucchini

AbstractA complex network of surveillance mechanisms, called checkpoints, interrupts cell cycle progression when damage to the genome is detected or when cells fail to complete DNA replication, thus ensuring genetic integrity. In budding yeast, components of the DNA damage checkpoint regulatory network include the RAD9, RAD17, RAD24, MEC3, DDC1, RAD53, and MEC1 genes that are proposed to be involved in different aspects of DNA metabolism. We provide evidence that some DNA damage checkpoint components play a role in maintaining telomere integrity. In fact, rad53 mutants specifically enhance repression of telomere-proximal transcription via the Sir-mediated pathway, suggesting that Rad53 might be required for proper chromatin structure at telomeres. Moreover, Rad53, Mec1, Ddc1, and Rad17 are necessary for telomere length maintenance, since mutations in all of these genes cause a decrease in telomere size. The telomeric shortening in rad53 and mec1 mutants is further enhanced in the absence of SIR genes, suggesting that Rad53/Mec1 and Sir proteins contribute to chromosome end protection by different pathways. The finding that telomere shortening, but not increased telomeric repression of gene expression in rad53 mutants, can be suppressed by increasing dNTP synthetic capacity in these strains suggests that transcriptional silencing and telomere integrity involve separable functions of Rad53.


1998 ◽  
Vol 17 (19) ◽  
pp. 5525-5528 ◽  
Author(s):  
M. P. Longhese

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