The Response to Oxidative DNA Damage in Neurons: Mechanisms and Disease

Narciso, Laura; Parlanti, Eleonora; Racaniello, Mauro; Simonelli, Valeria; Cardinale, Alessio; Merlo, Daniela; Dogliotti, Eugenia

doi:10.1155/2016/3619274

Cited by 62 publications

(51 citation statements)

References 147 publications

(172 reference statements)

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“…DAVID bioinformatics analyses (DAVID 6.7) showed that the top biological processes in NPC-specific paused genes highlighted different aspects of catabolic processes and cell cycle (Figure 4B and 4E), functions that appear to be required for supporting the proliferative state of NPCs. Those of neuron-specific paused genes revealed enrichment of activities involving DNA damage response and repair and cellular stress responses (Figure 4C and 4F), functions important for maintaining the integrity of post-mitotic neuronal cells (Narciso et al, 2016; Pan et al, 2014). Interestingly, with respect to DNA damage response and repair, different groups of paused genes were identified between NPCs and neurons (Supplemental Table S5).…”

Section: Resultsmentioning

confidence: 99%

Dynamics of RNA Polymerase II Pausing and Bivalent Histone H3 Methylation during Neuronal Differentiation in Brain Development

Liu

Zhang

et al. 2017

Cell Reports

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Summary During cellular differentiation, genes important for differentiation are expected to be silent in stem/progenitor cells yet can be readily activated. RNA polymerase II (Pol II) pausing and bivalent chromatin marks are two paradigms suited for establishing such a poised state of gene expression, however, their specific contributions in development are not well understood. Here, we characterized Pol II pausing and H3K4me3/H3K27me3 marks in neural progenitor cells (NPCs) and their daughter neurons purified from the developing mouse cortex. We show that genes paused in NPCs or neurons are characteristic of respective cellular functions important for each cell type, although pausing and pause release was not correlated with gene activation. Bivalent chromatin marks poised the marked genes in NPCs for activation in neurons. Interestingly, we observed a positive correlation between H3K27me3 and paused Pol II. This study thus reveals cell-type specific Pol II pausing and gene activation-associated bivalency during mammalian neuronal differentiation.

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Section: Resultsmentioning

confidence: 99%

Dynamics of RNA Polymerase II Pausing and Bivalent Histone H3 Methylation during Neuronal Differentiation in Brain Development

Liu

Zhang

et al. 2017

Cell Reports

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“…Mechanisms to repair the inevitable DNA damage associated with exposure to endogenous and exogenous agents are critical to the development and function of the nervous system as well as to protection against development of diseases, such as cancer (Cha & Yim, 2013; Curtin, 2012; Narciso et al, 2016; Smetana et al, 2016). Cancer and cancer treatment can initiate DNA damage and reduction in the effectiveness of some DNA repair mechanisms (Cha & Yim, 2013).…”

Section: Discussionmentioning

confidence: 99%

Trajectories of Cognitive Function and Associated Phenotypic and Genotypic Factors in Breast Cancer

Bender¹,

Merriman²,

Sereika³

et al. 2018

ONF

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OBJECTIVES This study identified women with unique trajectories of executive function, concentration, and visual working memory before and during adjuvant therapy for breast cancer, and examined phenotypic and genotypic predictors associated with subgroups. SAMPLE & SETTING 399 postmenopausal women, of whom 288 were women with early-stage breast cancer and 111 were women without breast cancer, matched on age and years of education to the women with breast cancer, and all at an urban cancer center. METHODS & VARIABLES A repeated-measures design was used; assessments occurred before adjuvant therapy and every six months post-therapy initiation. Group-based trajectory modeling determined subgroups. Multinomial logistic regression identified phenotypic and genotypic characteristics. RESULTS Three executive function and concentration trajectory subgroups were identified: low, moderate, and high; two visual working memory subgroups were identified: low and high. IMPLICATIONS FOR NURSING Advancing age, greater pretherapy fatigue, and poorer pretherapy cognitive function are associated with the low subgroups. DNA repair and oxidative stress mechanisms may be involved in the cognitive changes that women experience.

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“…The differentiation-driven switch in prioritizing TC-NER over GG-NER is still a mystery. Curiously, in various terminally differentiated cells, such as neurons and macrophages, damage is repaired with equal efficiency in both the transcribed strand of active genes and the non-transcribed strand [118][119][120]. This phenomenon, known as ‘transcription domain-associated repair’ is not yet understood.…”

Section: Future Challengesmentioning

confidence: 99%

Mechanistic insights into transcription coupled DNA repair

Pani

Nudler

2017

DNA Repair

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Transcription-coupled DNA repair (TCR) acts on lesions in the transcribed strand of active genes. Helix distorting adducts and other forms of DNA damage often interfere with the progression of the transcription apparatus. Prolonged stalling of RNA polymerase can promote genome instability and also induce cell cycle arrest and apoptosis. These generally unfavorable events are counteracted by RNA polymerase-mediated recruitment of specific proteins to the sites of DNA damage to perform TCR and eventually restore transcription. In this perspective we discuss the decision-making process to employ TCR and we elucidate the intricate biochemical pathways leading to TCR in E. coli and human cells.

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The Response to Oxidative DNA Damage in Neurons: Mechanisms and Disease

Cited by 62 publications

References 147 publications

Dynamics of RNA Polymerase II Pausing and Bivalent Histone H3 Methylation during Neuronal Differentiation in Brain Development

Dynamics of RNA Polymerase II Pausing and Bivalent Histone H3 Methylation during Neuronal Differentiation in Brain Development

Trajectories of Cognitive Function and Associated Phenotypic and Genotypic Factors in Breast Cancer

Mechanistic insights into transcription coupled DNA repair

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