8-Oxoguanine DNA glycosylase 1 (ogg1) maintains the function of cardiac progenitor cells during heart formation in zebrafish

Yan, Lifeng; Zhou, Yong; Yu, Shanhe; Ji, Guixiang; Wang, Lei; Liu, Wei; Gu, Aihua

doi:10.1016/j.yexcr.2013.07.012

Cited by 17 publications

(11 citation statements)

References 31 publications

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“…1 B, left panel). The distribution of NF-κB enrichment peaks are in line with previous observations [48] . Strikingly, the distribution of OGG1 enrichment peaks are similar to those of NF-κB at 1000 bp or longer (2000, or 10,000 bp ± TSS) genomic region ( Fig.…”

Section: Resultssupporting

confidence: 92%

“…1 D). These results together are supported by data that showed an increased susceptibility to obesity and related pathologies [16] , [17] , aberrant innate and adaptive immune responses in Ogg1 -/- mice [13] , [14] , [19] , [46] , developmental abnormalities of the central nervous and cardiovascular system in Ogg1 deficient zebrafish [47] , [48] , and aging processes [49] .…”

Section: Resultssupporting

confidence: 71%

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Effects of the stimuli-dependent enrichment of 8-oxoguanine DNA glycosylase1 on chromatinized DNA

Hao

Pan

et al. 2018

Redox Biology

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8-Oxoguanine DNA glycosylase 1 (OGG1) initiates the base excision repair pathway by removing one of the most abundant DNA lesions, 8-oxo-7,8-dihydroguanine (8-oxoG). Recent data showed that 8-oxoG not only is a pro-mutagenic genomic base lesion, but also functions as an epigenetic mark and that consequently OGG1 acquire distinct roles in modulation of gene expression. In support, lack of functional OGG1 in Ogg1-/- mice led to an altered expression of genes including those responsible for the aberrant innate and adaptive immune responses and susceptibility to metabolic disorders. Therefore, the present study examined stimulus-driven OGG1-DNA interactions at whole genome level using chromatin immunoprecipitation (ChIP)-coupled sequencing, and the roles of OGG1 enriched on the genome were validated by molecular and system-level approaches. Results showed that signaling levels of cellular ROS generated by TNFα, induced enrichment of OGG1 at specific sites of chromatinized DNA, primarily in the regulatory regions of genes. OGG1-ChIP-ed genes are associated with important cellular and biological processes and OGG1 enrichment was limited to a time scale required for immediate cellular responses. Prevention of OGG1-DNA interactions by siRNA depletion led to modulation of NF-κB's DNA occupancy and differential expression of genes. Taken together these data show TNFα-ROS-driven enrichment of OGG1 at gene regulatory regions in the chromatinized DNA, which is a prerequisite to modulation of gene expression for prompt cellular responses to oxidant stress.

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Section: Resultssupporting

confidence: 92%

Section: Resultssupporting

confidence: 71%

Effects of the stimuli-dependent enrichment of 8-oxoguanine DNA glycosylase1 on chromatinized DNA

Hao

Pan

et al. 2018

Redox Biology

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“…However, it is also important to consider that Nrf2 and its family members are also essential regulators of embryonic development, controlling erythropoiesis and angiogenesis (Shivdasani and Orkin, 1995; Wei et al, 2013; Williams et al, 2013). Likewise, Ogg1 has recently been shown to regulate embryonic cell proliferation and differentiation (Reis and Hermanson, 2012; Yan et al, 2013). In addition, one possible explanation may lie with ROS itself.…”

Section: Discussionmentioning

confidence: 99%

The cellular and molecular progression of mitochondrial dysfunction induced by 2,4-dinitrophenol in developing zebrafish embryos

et al. 2015

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The etiology of mitochondrial disease is poorly understood. Furthermore, treatment options are limited, and diagnostic methods often lack the sensitivity to detect disease in its early stages. Disrupted oxidative phosphorylation (OXPHOS) that inhibits ATP production is a common phenotype of mitochondrial disorders that can be induced in zebrafish by exposure to 2,4-dinitrophenol (DNP), a FDA-banned weight-loss agent and EPA-regulated environmental toxicant, traditionally used in research labs as an uncoupler of OXPHOS. Despite the DNP-induced OXPHOS inhibition we observed using in vivo respirometry, the development of the DNP-treated and control zebrafish were largely similar during the first half of embryogenesis. During this period, DNP-treated embryos induced gene expression of mitochondrial and nuclear genes that stimulated the production of new mitochondria and increased glycolysis to yield normal levels of ATP. DNP-treated embryos were incapable of sustaining this mitochondrial biogenic response past mid-embryogenesis, as shown by significantly lowered ATP production and ATP levels, decreased gene expression, and the onset of developmental defects. Examining neural tissues commonly affected by mitochondrial disease, we found that DNP exposure also inhibited motor neuron axon arbor outgrowth and the proper formation of the retina. We observed and quantified the molecular and physiological progression of mitochondrial dysfunction during development with this new model of OXPHOS dysfunction, which has great potential for use in diagnostics and therapies for mitochondrial disease.

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“…Zebrafish embryos in which Apex1 has been knocked down completely arrest at the midblastula transition (MBT), when zygotic transcription is initiated and differentiation begins. Embryos in which the Apex1 or Ogg1 protein has been partially knocked down (hypomorphs) show defective brain and heart development 16,17 .…”

Section: Introductionmentioning

confidence: 99%

AP endonuclease 1 (Apex1) influences brain development linking oxidative stress and DNA repair

et al. 2019

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Brain and neurons are particularly sensitive to reactive oxygen species (ROS). Oxidative damage from ROS results in increased 8-oxoguanine in DNA followed by repair through the base excision repair (BER) pathway. We reported earlier that AP endonuclease 1 (Apex1) not only participates directly in BER but also regulates transcription factor Creb1. Here, we investigated how Apex1 affects brain to respond effectively to oxidative damage during zebrafish development. Loss of Apex1 resulted in increased ROS, 8-oxoguanine, and abasic sites as well as loss of Ogg1, which recognizes 8-oxoguanine and is required for its repair. Moreover, knock-down of Apex1 not only resulted in reduction of expression of several major proteins in the BER pathway (Polb and Ogg1), and it also resulted in maldistribution and loss of four key brain transcription factors ( fezf2 , otx2 , egr2a , and pax2a ), leading to abnormal brain development. These results were independent of p53 protein level. In contrast, exposure to exogenous H 2 O 2 resulted in increased transcription and protein of Apex1 along with other BER components, as well as Creb1. Taken together, these results indicate that oxidative stress increased when the level of Apex1 was reduced, revealing a novel pathway of how Apex1 manages oxidative stress in developing brain.

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8-Oxoguanine DNA glycosylase 1 (ogg1) maintains the function of cardiac progenitor cells during heart formation in zebrafish

Cited by 17 publications

References 31 publications

Effects of the stimuli-dependent enrichment of 8-oxoguanine DNA glycosylase1 on chromatinized DNA

Effects of the stimuli-dependent enrichment of 8-oxoguanine DNA glycosylase1 on chromatinized DNA

The cellular and molecular progression of mitochondrial dysfunction induced by 2,4-dinitrophenol in developing zebrafish embryos

AP endonuclease 1 (Apex1) influences brain development linking oxidative stress and DNA repair

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