scholarly journals Rad50 Zinc Hook Is Important for the Mre11 Complex to Bind Chromosomal DNA Double-stranded Breaks and Initiate Various DNA Damage Responses

2012 ◽  
Vol 287 (38) ◽  
pp. 31747-31756 ◽  
Author(s):  
Jing He ◽  
Linda Z. Shi ◽  
Lan N. Truong ◽  
Chi-Sheng Lu ◽  
Niema Razavian ◽  
...  
2020 ◽  
Author(s):  
Jared J. Luxton ◽  
Miles J. McKenna ◽  
Lynn E. Taylor ◽  
Kerry A. George ◽  
Sara Zwart ◽  
...  

2015 ◽  
Vol 15 (6) ◽  
pp. 533-541 ◽  
Author(s):  
Jinlu Ma ◽  
Dan Zhang ◽  
Xia Ying ◽  
Ying Zhao ◽  
Chenchen He ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Munetoshi Maeda ◽  
Masanori Tomita ◽  
Mika Maeda ◽  
Hideki Matsumoto ◽  
Noriko Usami ◽  
...  

AbstractWe recently showed that when a low X-ray dose is used, cell death is enhanced in nucleus-irradiated compared with whole-cell-irradiated cells; however, the role of the cytoplasm remains unclear. Here, we show changes in the DNA damage responses with or without X-ray microbeam irradiation of the cytoplasm. Phosphorylated histone H2AX foci, a surrogate marker for DNA double-strand breaks, in V79 and WI-38 cells are not observed in nucleus irradiations at ≤ 2 Gy, whereas they are observed in whole-cell irradiations. Addition of an ataxia telangiectasia mutated (ATM) kinase inhibitor to whole-cell irradiations suppresses foci formation at ≤ 2 Gy. ABL1 and p73 expression is upregulated following nucleus irradiation, suggesting the induction of p73-dependent cell death. Furthermore, CDKN1A (p21) is upregulated following whole-cell irradiation, indicating the induction of cell cycle arrest. These data reveal that cytoplasmic radioresponses modify ATM-mediated DNA damage responses and determine the fate of cells irradiated at low doses.


Genetics ◽  
1998 ◽  
Vol 148 (3) ◽  
pp. 1055-1067
Author(s):  
Steven D Harris ◽  
Peter R Kraus

Abstract In Aspergillus nidulans, germinating conidia undergo multiple rounds of nuclear division before the formation of the first septum. Previous characterization of temperature-sensitive sepB and sepJ mutations showed that although they block septation, they also cause moderate defects in chromosomal DNA metabolism. Results presented here demonstrate that a variety of other perturbations of chromosomal DNA metabolism also delay septum formation, suggesting that this is a general cellular response to the presence of sublethal DNA damage. Genetic evidence is provided that suggests that high levels of cyclin-dependent kinase (cdk) activity are required for septation in A. nidulans. Consistent with this notion, the inhibition of septum formation triggered by defects in chromosomal DNA metabolism depends upon Tyr-15 phosphorylation of the mitotic cdk p34nimX. Moreover, this response also requires elements of the DNA damage checkpoint pathway. A model is proposed that suggests that the DNA damage checkpoint response represents one of multiple sensory inputs that modulates p34nimX activity to control the timing of septum formation.


2010 ◽  
Vol 29 (18) ◽  
pp. 3130-3139 ◽  
Author(s):  
Sophie E Polo ◽  
Abderrahmane Kaidi ◽  
Linda Baskcomb ◽  
Yaron Galanty ◽  
Stephen P Jackson

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Vincent Caval ◽  
Rodolphe Suspène ◽  
Milana Shapira ◽  
Jean-Pierre Vartanian ◽  
Simon Wain-Hobson

2016 ◽  
Vol 136 (5) ◽  
pp. S101 ◽  
Author(s):  
S. Shaik ◽  
M. Pollet ◽  
J. Krutmann ◽  
T. Haarmann-Stemmann

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