Maintenance of genome stability in plants: repairing DNA double strand breaks and chromatin structure stability

Roy, Sujit

doi:10.3389/fpls.2014.00487

Cited by 57 publications

(49 citation statements)

References 39 publications

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“…The repair process in plants has been the focus of several reviews (Roth et al, 2012;Donà et al, 2013;Knoll et al, 2014a;Missirian et al, 2014). In this Update, we summarize recent literature describing the connection of repair and chromatin in plants, adding to earlier reviews (Balestrazzi et al, 2011;Zhu et al, 2011;Roy, 2014). Although plants are surprisingly much less investigated in this context when compared with other multicellular organisms, they are potentially rewarding for further research, as some repair-and chromatin-related genes have extended gene families, and several complete loss-of-function mutations that are lethal in animals are viable in plants.…”

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confidence: 94%

DNA Damage Repair in the Context of Plant Chromatin

Donà

Scheid

2015

Plant Physiol.

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The integrity of DNA molecules is constantly challenged. All organisms have developed mechanisms to detect and repair multiple types of DNA lesions. The basic principles of DNA damage repair (DDR) in prokaryotes and unicellular and multicellular eukaryotes are similar, but the association of DNA with nucleosomes in eukaryotic chromatin requires mechanisms that allow access of repair enzymes to the lesions. This is achieved by chromatin-remodeling factors, and their necessity for efficient DDR has recently been demonstrated for several organisms and repair pathways. Plants share many features of chromatin organization and DNA repair with fungi and animals, but they differ in other, important details, which are both interesting and relevant for our understanding of genome stability and genetic diversity. In this Update, we compare the knowledge of the role of chromatin and chromatin-modifying factors during DDR in plants with equivalent systems in yeast and humans. We emphasize plant-specific elements and discuss possible implications.A DNA molecule in a eukaryotic chromosome has a diameter of 2 nm but a length in the range of centimeters. Being 10 7 times longer than it is wide would make it highly sensitive to breakage if it were not organized in compact and dynamic chromatin, with nucleosomes as basic units followed by multiple higher order levels of organization. Within this packaging, replication and transcription constitute an endogenous mechanical strain, while exposure of cells to physical or chemical hazard creates a wide range of DNA damage induced by external factors, including photoproducts, pyrimidine dimers, interstrand crosslinking, and single and double-strand breaks (DSBs). All organisms possess mechanisms that repair DNA molecules. DNA damage repair (DDR) systems for the various types of damage are overlapping as well as complementary, and their prevalence depends on the organism, the stage of the cell cycle, the site and the amount of damage, and the availability of intact templates. A coarse categorization distinguishes nucleotide excision repair, base excision repair, nonhomologous end joining (NHEJ), and homologous recombination (HR). Many schematic models for these DDR pathways describe the action and interaction of several repair components, but they are usually misleading in one aspect: DNA strands are illustrated as straight lines, neglecting the emerging role of chromatin for the location and the fate of DNA lesions. More realistically, we should envisage DNA lesions in the chromatin context like the leakage or burst of an in-ground pipe. Recognizing the defect, localizing it, excavating the broken parts, cleaning the ends, reconnecting them, and restoring the original state are mirrored in the subsequent steps of DDR: signaling, labeling, accessing, resecting, religating, and reassembling. Chromatin is expected to especially affect the access, resection, and restoration of the original arrangement, and several factors that can dissolve higher order structures, slide, evict, or exchange ...

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confidence: 94%

DNA Damage Repair in the Context of Plant Chromatin

Donà

Scheid

2015

Plant Physiol.

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“…Innate immunity is a non-toxic mechanism to fight intruders and diseased cell via genomic mechanisms and gene repair [8,45]. Classical markers of innate immunity like the NFkB, MAPkinase, BAX and c-jun have been recognized as key markers for cell repair and new markers like the VEGF gene and many others have been added in the evolutionary process as expansions and adaptations.…”

Section: Discussionmentioning

confidence: 99%

“…Understanding biotic (parasite) or abiotic (drought) stress on plants is of tremendous importance. Plants can detect environmental changes and respond to stress to conserve resources for growth and reproduction through activating a unique stress DNA repair response, which was conserved from yeasts [8,45].…”

Section: Genomic Stability In Nutritional Plantsmentioning

confidence: 99%

“…Plants also have MAPkinase components, with a wide range of stress response cascades [45] for biotic stress of pathogen response, abiotic stress mediates other MAPkinase cascades.…”

Section: Genomic Stability In Nutritional Plantsmentioning

confidence: 99%

“…BAX gene expression is part of yeasts and plant gene expression as part of the innate immunity stress defense, where a dead cell layer is created inhibiting the intruder from entering the living cell and forcing the intruder to move over a defense layer of dead cells [8,45]. This active defense mechanism is used to end pregnancy, as there is a strong increase of BAX expression in preeclampsia placentas compared to the normal full-term placentas, suggesting that deregulation of apoptotic turn over may lead to placental dysfunction and pathologies [28].…”

Section: The Bax Genementioning

confidence: 99%

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The evolution of genomic stability to a mechanism in reproduction and psychiatry

Regidor

Volko

Schindler³

et al. 2016

Hormone Molecular Biology and Clinical Investigation

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There are two forms of immune defense, the specific or adaptive immune defense and the unspecific innate immune defense. Vaccination is utilized against specific bacteria via the adaptive immune system. The innate immunity DNA stress defense is a non-toxic mechanism developed in yeasts and conserved in mammals and in plants. Although the steroidal hormone cascade has overtaken the stress response and allows superfast response via non-genomic receptors, the old innate immunity response is still mediated via the steroidal hormones cascade. The classical drug/receptor model has provided for many solutions, however, in antibiotics, cancer, and in severe mental diseases this model reaches to certain limits. The NIH/Department of Mental Health has developed a new model that shows severe mental diseases may be immune diseases that can be treated by replacing old diseased nerve cells by new healthy nerve cells, where the old innate immunity may be exploited. This means that severe mental diseases are physical diseases. A newly developed model, where modifications of the steroidal hormone cascade help to understand bipolarity, schizophrenia, and PTSD in men and women can be transferred to gynecological hormone modifications in women, where innate immunity is mediated via the same steroidal hormone cascade. Treatment via immune response via the DNA cascade should be developed in cancer, infections and severe mental disease, because foreign cells or diseased cells may be removed by the unspecific innate immunity.

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Impact of UV Radiation on Genome Stability and Human Health

Roy

2017

Advances in Experimental Medicine and Biology

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Gradual depletion of the atmospheric ozone layer during the past few years has increased the incidence of solar UV radiation specifically the UV-C on earth's surface is one of the major environmental concerns because of the harmful effects of this radiation in all forms of life. The solar UV radiation including the harmful wavelength range of UV-B (280-320 nm) represents a significant climatic stress for both animals and plants, causing damage to the fundamental biomolecules such as DNA, proteins and lipids, thus activating genotoxic stress and induces genome instability. When DNA absorbs UV-B light, energy from the photon causes covalent linkages to form between adjacent pyrimidine bases, creating photoproducts, primarily cyclobutane pyrimidine dimers (CPDs) and pyrimidine-6,4-pyrimidinone photoproduct (6,4PPs). Pyrimidine dimers create distortions in the DNA strands and therefore can inhibit DNA replication as well transcription. Lack of efficient repair of UV-induced DNA damage may induce the formation of DNA double stand breaks (DSBs), one of the serious forms of damage in DNA double helix, as well as oxidative damage. Unrepaired DSBs in the actively dividing somatic cells severely affect cell growth and development, finally results in loss of cell viability and development of various diseases, such as cancer in man.This chapter mainly highlights the incidence of solar UV-radiation on earth's surface along with the formation of major types of UV-induced DNA damage and the associated repair mechanisms as well as methods of detecting DNA damage and finally our present understanding on the impact on solar UV radiation on human health.

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Maintenance of genome stability in plants: repairing DNA double strand breaks and chromatin structure stability

Cited by 57 publications

References 39 publications

DNA Damage Repair in the Context of Plant Chromatin

DNA Damage Repair in the Context of Plant Chromatin

The evolution of genomic stability to a mechanism in reproduction and psychiatry

Impact of UV Radiation on Genome Stability and Human Health

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