scholarly journals Overexpression of rice jacalin-related mannose-binding lectin (OsJAC1) enhances resistance to ionizing radiation in Arabidopsis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
In Jung Jung ◽  
Joon-Woo Ahn ◽  
Sera Jung ◽  
Jung Eun Hwang ◽  
Min Jeong Hong ◽  
...  
Keyword(s):  
Dna Damage ◽  
Gamma Radiation ◽  
Expression Profiles ◽  
Dna Damage Checkpoints ◽  
Damage Response ◽  
Mannose Binding ◽  
Transgenic Lines ◽  
Dose Dependent ◽  
Resistance To Ionizing Radiation ◽  
Binding Lectin

Abstract Background Jacalin-related lectins in plants are important in defense signaling and regulate growth, development, and response to abiotic stress. We characterized the function of a rice mannose-binding jacalin-related lectin (OsJAC1) in the response to DNA damage from gamma radiation. Results Time- and dose-dependent changes of OsJAC1 expression in rice were detected in response to gamma radiation. To identify OsJAC1 function, OsJAC1-overexpressing transgenic Arabidopsis plants were generated. Interestingly, OsJAC1 overexpression conferred hyper-resistance to gamma radiation in these plants. Using comparative transcriptome analysis, genes related to pathogen defense were identified among 22 differentially expressed genes in OsJAC1-overexpressing Arabidopsis lines following gamma irradiation. Furthermore, expression profiles of genes associated with the plant response to DNA damage were determined in these transgenic lines, revealing expression changes of important DNA damage checkpoint and perception regulatory components, namely MCMs, RPA, ATM, and MRE11. Conclusions OsJAC1 overexpression may confer hyper-resistance to gamma radiation via activation of DNA damage perception and DNA damage checkpoints in Arabidopsis, implicating OsJAC1 as a key player in DNA damage response in plants. This study is the first report of a role for mannose-binding jacalin-related lectin in DNA damage.

Alterations in gene expression profiles and the DNA-damage response in ionizing radiation-exposed TK6 cells

2005 ◽  
Vol 45 (2-3) ◽  
pp. 188-205 ◽  
Author(s):  
Gregory S. Akerman ◽  
Barry A. Rosenzweig ◽  
Olen E. Domon ◽  
Chen-An Tsai ◽  
Michelle E. Bishop ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Damage ◽  
Ionizing Radiation ◽  
Dna Damage Response ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Damage Response ◽  
Tk6 Cells

scholarly journals Cisplatin-induced peripheral neuropathy is associated with neuronal senescence-like response

2020 ◽  
Author(s):  
Aina Calls ◽  
Abel Torres-Espin ◽  
Xavier Navarro ◽  
Victor J Yuste ◽  
Esther Udina ◽  
...  
Keyword(s):  
Dna Damage ◽  
Peripheral Neuropathy ◽  
Sensory Neurons ◽  
Neuronal Population ◽  
Protein Product ◽  
Damage Response ◽  
Neuroprotective Treatment ◽  
Activation Pathways ◽  
Dose Dependent

Abstract Background Cisplatin-induced peripheral neuropathy (CIPN) is a frequent serious dose-dependent adverse event that can determine dosage limitations for cancer treatment. CIPN severity correlates with the amount of platinum detected in sensory neurons of the dorsal root ganglia (DRG). However, the exact pathophysiology of CIPN is poorly understood, so the chance of developing neuroprotective treatment is reduced. The aim of this study was to determine the exact mechanisms involved in CIPN development. Methods By single-cell RNA-sequencing (scRNAseq), we have studied the transcriptomic profile of DRG sensory neurons from a well-characterized neurophysiological mouse model of CIPN. Results Gene Ontology analysis of the scRNAseq data indicated that cisplatin treatment induces the upregulation of biological pathways related to DNA damage response (DDR) in the DRG neuronal population. Moreover, DRG neurons also upregulated the Cdkn1a gene, confirmed later by the measurement of its protein product p21. While apoptosis activation pathways were not observed in DRG sensory neurons of cisplatin-treated mice, these neurons did express several senescence hallmarks, including senescence-associated β-galactosidase, phospho-H2AX, and nuclear factor kappa B (Nfkb)–p65 proteins. Conclusions In this study, we determined that after cisplatin-induced DNA damage, p21 appears as the most relevant downstream factor of the DDR in DRG sensory neurons in vivo, which survive in a nonfunctional senescence-like state.

Dose-dependent influence of genetic polymorphisms on DNA damage induced by styrene oxide, ethylene oxide and gamma-radiation

Toxicology ◽  
2006 ◽  
Vol 219 (1-3) ◽  
pp. 220-229 ◽  
Author(s):  
Lode Godderis ◽  
Peter Aka ◽  
Raluca Mateuca ◽  
Micheline Kirsch-Volders ◽  
Dominique Lison ◽  
...  
Keyword(s):  
Dna Damage ◽  
Ethylene Oxide ◽  
Gamma Radiation ◽  
Genetic Polymorphisms ◽  
Styrene Oxide ◽  
Dose Dependent

scholarly journals Generation and Characterization of Transgenic Plum Lines Expressing gafp-1 with the bul409 Promoter

HortScience ◽  
2011 ◽  
Vol 46 (7) ◽  
pp. 975-980 ◽  
Author(s):  
Hetal M. Kalariya ◽  
Guido Schnabel ◽  
Cesar Petri ◽  
Ralph Scorza
Keyword(s):  
Root Rot ◽  
Woody Plants ◽  
Antifungal Protein ◽  
Open Pollination ◽  
Root Knot Nematode ◽  
Phytophthora Root Rot ◽  
Mannose Binding ◽  
Transgenic Lines ◽  
Binding Lectin

The Gastrodia antifungal protein (GAFP-1) is a mannose-binding lectin that can confer increased disease resistance in transgenic tobacco and plum. In all previously generated, transgenic lines, the gene was under the control of the 35SCaMV promoter. In this study, transgenic plum lines were created from seeds derived from open pollination of the cultivar Bluebyrd (BB-OP) with gafp-1 under the control of the polyubiquitin promoter bul409 and evaluated for Phytophthora root rot (PRR) and Root knot nematode (RKN) susceptibility. One of nine transgenic lines synthesizing GAFP-1 exhibited increased tolerance to PRR caused by P. cinnamomi. The same line (BB-OP-1) was also significantly more tolerant to RKN infection caused by Meloidogyne incognita. BB-OP-1 was more resistant to PRR and equally resistant to RKN compared with the cultivar Stanley-derived 4J line, which expresses gafp-1 under the control of the 35SCaMV promoter. GAFP-1 synthesis in BB-OP-1 was not elevated by pathogen infection, suggesting that the bul409 promoter is not inducible in the plum/GAFP-1 system. This study confirms the usefulness of the gafp-1 gene in various cultivars of transgenic plum and establishes that the bul409 promoter is at least equal in effectiveness to the 35SCaMV promoter for gafp-1 expression in transgenic lines of woody plants.

Transcription profile of DNA damage response genes at G0 lymphocytes exposed to gamma radiation

2012 ◽  
Vol 364 (1-2) ◽  
pp. 271-281 ◽  
Author(s):  
Divyalakshmi Saini ◽  
Shridevi Shelke ◽  
A. Mani Vannan ◽  
Sneh Toprani ◽  
Vinay Jain ◽  
...  
Keyword(s):  
Dna Damage ◽  
Gamma Radiation ◽  
Dna Damage Response ◽  
Transcription Profile ◽  
Damage Response

scholarly journals Telomerase Is Essential to Alleviate Pif1-Induced Replication Stress at Telomeres

Genetics ◽  
2009 ◽  
Vol 183 (3) ◽  
pp. 779-791 ◽  
Author(s):  
Michael Chang ◽  
Brian Luke ◽  
Claudine Kraft ◽  
Zhijian Li ◽  
Matthias Peter ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Dna Damage Response ◽  
Response Factors ◽  
Growth Defects ◽  
Evolutionarily Conserved ◽  
Damage Response ◽  
Complete Set ◽  
Dependent Growth ◽  
Dose Dependent

Pif1, an evolutionarily conserved helicase, negatively regulates telomere length by removing telomerase from chromosome ends. Pif1 has also been implicated in DNA replication processes such as Okazaki fragment maturation and replication fork pausing. We find that overexpression of Saccharomyces cervisiae PIF1 results in dose-dependent growth inhibition. Strong overexpression causes relocalization of the DNA damage response factors Rfa1 and Mre11 into nuclear foci and activation of the Rad53 DNA damage checkpoint kinase, indicating that the toxicity is caused by accumulation of DNA damage. We screened the complete set of ∼4800 haploid gene deletion mutants and found that moderate overexpression of PIF1, which is only mildly toxic on its own, causes growth defects in strains with mutations in genes involved in DNA replication and the DNA damage response. Interestingly, we find that telomerase-deficient strains are also sensitive to PIF1 overexpression. Our data are consistent with a model whereby increased levels of Pif1 interfere with DNA replication, causing collapsed replication forks. At chromosome ends, collapsed forks result in truncated telomeres that must be rapidly elongated by telomerase to maintain viability.

scholarly journals The Time for Chronotherapy in Radiation Oncology

2021 ◽  
Vol 11 ◽  
Author(s):  
Luis Bermúdez-Guzmán ◽  
Alejandro Blanco-Saborío ◽  
Juliana Ramírez-Zamora ◽  
Eduardo Lovo
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Therapeutic Potential ◽  
Working Hours ◽  
Experimental Models ◽  
Time Range ◽  
Repair Enzymes ◽  
Dna Damage Checkpoints ◽  
Damage Response ◽  
Treatment Administration

Five decades ago, Franz Halberg conceived the idea of ​​a circadian-based therapy for cancer, given the differential tolerance to treatment derived from the intrinsic host rhythms. Nowadays, different experimental models have demonstrated that both the toxicity and efficacy of several anticancer drugs vary by more than 50% as a function of dosing time. Accordingly, it has been shown that chemotherapeutic regimens optimally timed with the circadian cycle have jointly improved patient outcomes both at the preclinical and clinical levels. Along with chemotherapy, radiation therapy is widely used for cancer treatment, but its effectiveness relies mainly on its ability to damage DNA. Notably, the DNA damage response including DNA repair, DNA damage checkpoints, and apoptosis is gated by the circadian clock. Thus, the therapeutic potential of circadian-based radiotherapy against cancer is mainly dependent upon the control that the molecular clock exerts on DNA repair enzymes across the cell cycle. Unfortunately, the time of treatment administration is not usually considered in clinical practice as it varies along the daytime working hours. Currently, only a few studies have evaluated whether the timing of radiotherapy affects the treatment outcome. Several of these studies show that it is possible to reduce the toxicity of the treatment if it is applied at a specific time range, although with some inconsistencies. In this Perspective, we review the main advances in the field of chronoradiotherapy, the possible causes of the inconsistencies observed in the studies so far and provide some recommendations for future trials.

scholarly journals Exploring microRNA Signatures of DNA Damage Response Using an Innovative System of Genotoxic Stress in Medicago truncatula Seedlings

2021 ◽  
Vol 12 ◽  
Author(s):  
Carla Gualtieri ◽  
Maraeva Gianella ◽  
Andrea Pagano ◽  
Tiziano Cadeddu ◽  
Susana Araújo ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Medicago Truncatula ◽  
Dna Damage Response ◽  
Topoisomerase I ◽  
Expression Profiles ◽  
Indirect Evidence ◽  
Genotoxic Stress ◽  
Model Legume ◽  
Damage Response

One of the challenges that living organisms face is to promptly respond to genotoxic stress to avoid DNA damage. To this purpose, all organisms, including plants, developed complex DNA damage response (DDR) mechanisms. These mechanisms are highly conserved among organisms and need to be finely regulated. In this scenario, microRNAs (miRNAs) are emerging as active players, thus attracting the attention of the research community. The involvement of miRNAs in DDR has been investigated prominently in human cells whereas studies in plants are still scarce. To experimentally investigate the involvement of plant miRNAs in the regulation of DDR-associated pathways, an ad hoc system was developed, using the model legume Medicago truncatula. Specific treatments with camptothecin (CPT) and/or NSC120686 (NSC), targeting distinct components of DDR, namely topoisomerase I (TopI) and tyrosyl-DNA phosphodiesterase 1 (TDP1), were used. Phenotypic (germination percentage and speed, seedling growth) and molecular (cell death, DNA damage, and gene expression profiles) analyses demonstrated that the imposed treatments impact DDR. Our results show that these treatments do not influence the germination process but rather inhibit seedling development, causing an increase in cell death and accumulation of DNA damage. Moreover, treatment-specific changes in the expression of suppressor of gamma response 1 (SOG1), master-regulator of plant DDR, were observed. Additionally, the expression of multiple genes playing important roles in different DNA repair pathways and cell cycle regulation were differentially expressed in a treatment-specific manner. Subsequently, specific miRNAs identified from our previous bioinformatics approaches as putatively targeting genes involved in DDR processes were investigated alongside their targets. The obtained results indicate that under most conditions when a miRNA is upregulated the corresponding candidate target gene is downregulated, providing an indirect evidence of miRNAs action over these targets. Hence, the present study extends the present knowledge on the information available regarding the roles played by miRNAs in the post-transcriptional regulation of DDR in plants.

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