scholarly journals Budding yeast 14-3-3 proteins contribute to the robustness of the DNA damage and spindle checkpoints

Cell Cycle ◽  
2008 ◽  
Vol 7 (17) ◽  
pp. 2749-2761 ◽  
Author(s):  
Nathalie Grandin ◽  
Michel Charbonneau
Keyword(s):  
Dna Damage ◽  
Budding Yeast ◽  
Spindle Checkpoints

A peptide derived from GAPDH enhances resistance to DNA damage in budding yeast

2021 ◽  
Author(s):  
Xi Zhao ◽  
Xianqiang Lian ◽  
Yan Liu ◽  
Liyan Zhou ◽  
Bian Wu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Common Good ◽  
Budding Yeast ◽  
Social Activity ◽  
Social Behaviors ◽  
Research Field ◽  
Yeast Cells ◽  
The Social ◽  
The Common ◽  
Established Role

Social behaviors do not only exist in higher organisms but are also present in microbes that interact for the common good. Here, we report that budding yeast cells interact with their neighboring cells after exposure to DNA damage. Yeast cells irradiated with DNA-damaging ultraviolet light secrete signal peptides that can increase the survival of yeast cells exposed to DNA-damaging stress. The secreted peptide is derived from glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and it induced cell death of a fraction of yeast cells in the group. The data suggest that the GAPDH-derived peptide serves in budding yeast’s social interaction in response to DNA-damaging stress. Importance Many studies have shown that microorganisms, including bacteria and yeast, display increased tolerance to stress after exposure to the same stressor. However, the mechanism remains unknown. In this manuscript, we report a striking finding that S. cerevisiae cells respond to DNA damage by secreting a peptide that facilitates resistance to DNA-damaging stress. Although it has been shown that GAPDH possesses many key functions in cells aside from its well-established role in glycolysis, this study demonstrated that GAPDH is also involved in the social behaviors response to DNA-damaging stress. The study opens the gate to an interesting research field about microbial social activity for adaptation to a harsh environment.

Fission yeast Pds5 is required for accurate chromosome segregation and for survival after DNA damage or metaphase arrest

2002 ◽  
Vol 115 (3) ◽  
pp. 587-598 ◽  
Author(s):  
Shao-Win Wang ◽  
Rebecca L. Read ◽  
Chris J. Norbury
Keyword(s):  
Dna Damage ◽  
Fission Yeast ◽  
Sister Chromatid ◽  
Budding Yeast ◽  
Eukaryotic Cell ◽  
Sister Chromatid Cohesion ◽  
Chromosome Loss ◽  
Dependent Manner ◽  
Yeast Saccharomyces Cerevisiae ◽  
Chromatid Cohesion

Sister chromatid cohesion, which is established during the S phase of the eukaryotic cell cycle and persists until the onset of anaphase, is essential for the maintenance of genomic integrity. Cohesion requires the multi-protein complex cohesin, as well as a number of accessory proteins including Pds5/BIMD/Spo76. In the budding yeast Saccharomyces cerevisiae Pds5 is an essential protein that localises to chromosomes in a cohesin-dependent manner. Here we describe the characterisation in the fission yeast Schizosaccharomyces pombe of pds5+, a novel,non-essential orthologue of S. cerevisiae PDS5. The S. pombePds5 protein was localised to punctate nuclear foci in a manner that was dependent on the Rad21 cohesin component. This, together with additional genetic evidence, points towards an involvement of S. pombe Pds5 in sister chromatid cohesion. S. pombe pds5 mutants were hypersensitive to DNA damage and to mitotic metaphase delay, but this sensitivity was apparently not due to precocious loss of sister chromatid cohesion. These cells also suffered increased spontaneous chromosome loss and meiotic defects and their viability was dependent on the spindle checkpoint protein Bub1. Thus, while S. pombe Pds5 has an important cohesin-related role, this differs significantly from that of the equivalent budding yeast protein.

Budding Yeast DNA Damage Checkpoint: A Signal Transduction-Mediated Surveillance System

2003 ◽  
pp. 197-202
Author(s):  
Marco Muzi-Falconi ◽  
Michele Giannattasio ◽  
Giordano Liberi ◽  
Achille Pelliccioli ◽  
Paolo Plevani ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Dna Damage ◽  
Surveillance System ◽  
Budding Yeast ◽  
Dna Damage Checkpoint

scholarly journals Involvement of deoxycytidylate deaminase in the response to Sn1-type methylation DNA damage in budding yeast

2007 ◽  
Vol 17 (17) ◽  
pp. R755-R757 ◽  
Author(s):  
R. Michael Liskay ◽  
Linda J. Wheeler ◽  
Christopher K. Mathews ◽  
Naz Erdeniz
Keyword(s):  
Dna Damage ◽  
Budding Yeast

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 ◽  
...  
Keyword(s):  
Dna Damage ◽  
Budding Yeast ◽  
Dna Damage Checkpoint

A novel role for the budding yeast RAD9 checkpoint gene in DNA damage-dependent transcription.

1996 ◽  
Vol 15 (15) ◽  
pp. 3912-3922 ◽  
Author(s):  
A. Aboussekhra ◽  
J. E. Vialard ◽  
D. E. Morrison ◽  
M. A. de la Torre-Ruiz ◽  
L. Cernáková ◽  
...  
Keyword(s):  
Dna Damage ◽  
Budding Yeast ◽  
Checkpoint Gene

scholarly journals Direct and Indirect Control of the Initiation of Meiotic Recombination by DNA Damage Checkpoint Mechanisms in Budding Yeast

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e65875 ◽  
Author(s):  
Bilge Argunhan ◽  
Sarah Farmer ◽  
Wing-Kit Leung ◽  
Yaroslav Terentyev ◽  
Neil Humphryes ◽  
...  
Keyword(s):  
Dna Damage ◽  
Meiotic Recombination ◽  
Budding Yeast ◽  
Dna Damage Checkpoint ◽  
Indirect Control

scholarly journals Phosphorylation of the Budding Yeast 9-1-1 Complex Is Required for Dpb11 Function in the Full Activation of the UV-Induced DNA Damage Checkpoint

2008 ◽  
Vol 28 (15) ◽  
pp. 4782-4793 ◽  
Author(s):  
Fabio Puddu ◽  
Magda Granata ◽  
Lisa Di Nola ◽  
Alessia Balestrini ◽  
Gabriele Piergiovanni ◽  
...  
Keyword(s):  
Dna Damage ◽  
Budding Yeast ◽  
Dna Damage Checkpoint ◽  
Checkpoint Activation ◽  
Checkpoint Response ◽  
Checkpoint Proteins ◽  
M Phase ◽  
Mutant Cells ◽  
Full Activation

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.

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