scholarly journals UV Damaged DNA Repair & Tolerance in Plants

Author(s):  
Ashwin L. ◽  
Dana F.
Keyword(s):  
BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Elisabetta Bassi ◽  
Paola Perucca ◽  
Isabella Guardamagna ◽  
Ennio Prosperi ◽  
Lucia A. Stivala ◽  
...  

Abstract Background The Host Cell Reactivation assay (HCR) allows studying the DNA repair capability in different types of human cells. This assay was carried out to assess the ability in removing UV-lesions from DNA, thus verifying NER efficiency. Previously we have shown that DDB2, a protein involved in the Global Genome Repair, interacts directly with PCNA and, in human cells, the loss of this interaction affects DNA repair machinery. In addition, a mutant form unable to interact with PCNA (DDB2PCNA-), has shown a reduced ability to interact with a UV-damaged DNA plasmid in vitro. Methods In this work, we have investigated whether DDB2 protein may influence the repair of a UV-damaged DNA plasmid into the cellular environment by applying the HCR method. To this end, human kidney 293 stable clones, expressing DDB2Wt or DDB2PCNA-, were co-transfected with pmRFP-N2 and UV-irradiated pEGFP-reported plasmids. Moreover, the co-localization between DDB2 proteins and different NER factors recruited at DNA damaged sites was analysed by immunofluorescence and confocal microscopy. Results The results have shown that DDB2Wt recognize and repair the UV-induced lesions in plasmidic DNA transfected in the cells, whereas a delay in these processes were observed in the presence of DDB2PCNA-, as also confirmed by the different extent of co-localization of DDB2Wt and some NER proteins (such as XPG), vs the DDB2 mutant form. Conclusion The HCR confirms itself as a very helpful approach to assess in the cellular context the effect of expressing mutant vs Wt NER proteins on the DNA damage response. Loss of interaction of DDB2 and PCNA affects negatively DNA repair efficiency.


2004 ◽  
Vol 24 (14) ◽  
pp. 6215-6230 ◽  
Author(s):  
Toru M. Nakamura ◽  
Li-Lin Du ◽  
Christophe Redon ◽  
Paul Russell

ABSTRACT Mammalian ATR and ATM checkpoint kinases modulate chromatin structures near DNA breaks by phosphorylating a serine residue in the carboxy-terminal tail SQE motif of histone H2AX. Histone H2A is similarly regulated in Saccharomyces cerevisiae. The phosphorylated forms of H2AX and H2A, known as γ-H2AX and γ-H2A, are thought to be important for DNA repair, although their evolutionarily conserved roles are unknown. Here, we investigate γ-H2A in the fission yeast Schizosaccharomyces pombe. We show that formation of γ-H2A redundantly requires the ATR/ATM-related kinases Rad3 and Tel1. Mutation of the SQE motif to AQE (H2A-AQE) in the two histone H2A genes caused sensitivity to a wide range of genotoxic agents, increased spontaneous DNA damage, and impaired checkpoint maintenance. The H2A-AQE mutations displayed a striking synergistic interaction with rad22Δ (Rad52 homolog) in ionizing radiation (IR) survival. These phenotypes correlated with defective phosphorylation of the checkpoint proteins Crb2 and Chk1 and a failure to recruit large amounts of Crb2 to damaged DNA. Surprisingly, the H2A-AQE mutations substantially suppressed the IR hypersensitivity of crb2Δ cells by a mechanism that required the RecQ-like DNA helicase Rqh1. We propose that γ-H2A modulates checkpoint and DNA repair through large-scale recruitment of Crb2 to damaged DNA. This function correlates with evidence that γ-H2AX regulates recruitment of several BRCA1 carboxyl terminus domain-containing proteins (NBS1, 53BP1, MDC1/NFBD1, and BRCA1) in mammals.


2019 ◽  
Author(s):  
Margaret R. Heider ◽  
Lixin Chen ◽  
Chen Song ◽  
Luo Sun ◽  
Pingfang Liu ◽  
...  

Plant Science ◽  
2015 ◽  
Vol 235 ◽  
pp. 101-110 ◽  
Author(s):  
Lanyang Gao ◽  
Shuzhang Yang ◽  
Yunye Zhu ◽  
Junfang Zhang ◽  
Ming Zhuo ◽  
...  

2012 ◽  
Vol 40 (2) ◽  
pp. 1505-1510 ◽  
Author(s):  
Jian Tie ◽  
Seisaku Uchigasaki

Sign in / Sign up

Export Citation Format

Share Document