Quantitative mechanisms of DNA damage sensing and signaling

Bantele, Susanne C. S.; Pfander, Boris

doi:10.1007/s00294-019-01007-4

Cited by 11 publications

(5 citation statements)

References 49 publications

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“…The "SOS response" in E. coli is initiated by accumulation of single-stranded DNA (ssDNA) during replication of DNA containing lesions (Maslowska et al, 2019). For both bacteria and eukaryotes, Bantele and Pfander (2019) propose a mechanism for responding to DNA damage that is based on the persistence of ssDNA: (1) repair locally if the damage level is low and ssDNA is short-lived; and (2) halt cell division until global repair of high-level damage is accomplished. The overall amount of ssDNA in a given cell must exceed a threshold to activate a DNA damage "checkpoint" for cell division.…”

Section: Damage and Repair Of Organellar Dnamentioning

confidence: 99%

Reactive Oxygen Species, Antioxidant Agents, and DNA Damage in Developing Maize Mitochondria and Plastids

et al. 2020

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Maize shoot development progresses from non-pigmented meristematic cells at the base of the leaf to expanded and non-dividing green cells of the leaf blade. This transition is accompanied by the conversion of promitochondria and proplastids to their mature forms and massive fragmentation of both mitochondrial DNA (mtDNA) and plastid DNA (ptDNA), collectively termed organellar DNA (orgDNA). We measured developmental changes in reactive oxygen species (ROS), which at high concentrations can lead to oxidative stress and DNA damage, as well as antioxidant agents and oxidative damage in orgDNA. Our plants were grown under normal, non-stressful conditions. Nonetheless, we found more oxidative damage in orgDNA from leaf than stalk tissues and higher levels of hydrogen peroxide, superoxide, and superoxide dismutase in leaf than stalk tissues and in light-grown compared to dark-grown leaves. In both mitochondria and plastids, activities of the antioxidant enzyme peroxidase were higher in stalk than in leaves and in dark-grown than light-grown leaves. In protoplasts, the amount of the small-molecule antioxidants, glutathione and ascorbic acid, and catalase activity were also higher in the stalk than in leaf tissue. The data suggest that the degree of oxidative stress in the organelles is lower in stalk than leaf and lower in dark than light growth conditions. We speculate that the damaged/fragmented orgDNA in leaves (but not the basal meristem) results from ROS signaling to the nucleus to stop delivering DNA repair proteins to mature organelles producing large amounts of ROS.

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Section: Damage and Repair Of Organellar Dnamentioning

confidence: 99%

Reactive Oxygen Species, Antioxidant Agents, and DNA Damage in Developing Maize Mitochondria and Plastids

et al. 2020

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“…Furthermore, gene body DNA methylation conspires with H3K36me3 to preclude aberrant transcription (47).DNA damage is related to the balance between survival and death in cancer biology (48).As exempli ed in diverse cancers,disruption or deregulation of DNA repair pathways results in genome instability (49).Moreover, the DNA mismatch repair triggers cell cycle arrest in some cases (50).The DNA damage respons makes it safe to play with knives (51). Cell fate regulation is associated with upon DNA damage (52,53). Intriguingly, we clearly identity that mutant MEG3 increases the telomeras activity dependent on DNA damage repair.…”

Section: Discussionmentioning

confidence: 99%

Mutant MEG3 Enhances the Activity of Telomerase by Increasing DNA Damage Repair in Human Liver Cancer Stem Cells

Song

Xie

Qin

et al. 2021

Preprint

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Background: Long noncoding RNAs have recently considered as central regulators in diverse biological processes and emerged as vital players controlling tumorigenesis. Although wild MEG3 acts as a suppressor in several cancers, the function of mutant MEG3 is also unclear during tumorigenesis.Methods: Lentivalus infection,RT-PCR,Western blotting and tumorigenesis test in vitro and in vivo were performed.Results: our results suggest that mutant MEG3 promotes the growth of human liver cancer stem cells in vivo and in vitro.Mechanistically, our results show that mutant MEG3 enhances acetylation modification of HistoneH4 on K16.Then, mutant MEG3 enhances the expression of SETD2 dependent on H4K16Ac.Moreover, mutant MEG3 increases the DNA damage repair through SETD2.Ultimately, mutant MEG3 increases the telomeras activity dependent on DNA damage repair.Strikingly,TERT determines the cancerous function of mutant MEG3 in liver cancer stem cells. Therefore, we shed light on the fact that targeting mutant MEG3 could be a viable approach for cancer treatment.Conclusions: these observations will play an important role in finding effective tumor treatment targets.

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“…The ATM-CHK2 and ATR-CHK1 axes also stimulate the transcriptional activity of p53, which promotes a temporary arrest in the cell cycle, thus allowing DNA repair and restoration of homeostasis [ 51 ]. Once the damage is repaired, all these post-translational modifications are reversed to stop the DDR signal [ 13 , 65 , 66 , 67 , 68 ] ( Figure 3 ).…”

Section: Molecular Pathways For Genome Stability Maintenancementioning

confidence: 99%

“…To face DNA damage, cells have evolved a complex set of mechanisms termed DNA damage response (DDR), which allows the detection of the lesions, activates the damage signaling, and regulates the DNA repair [ 13 , 14 ]. It has been suggested that E2 signaling inhibits the DDR to induce chromosomal instability and aneuploidy, which are typical cytogenetic prerequisites for BC initiation and progression [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

A Tale of Ice and Fire: The Dual Role for 17β-Estradiol in Balancing DNA Damage and Genome Integrity

Pescatori

Berardinelli

Albanesi

et al. 2021

Cancers

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17β-estradiol (E2) regulates human physiology both in females and in males. At the same time, E2 acts as a genotoxic substance as it could induce DNA damages, causing the initiation of cellular transformation. Indeed, increased E2 plasma levels are a risk factor for the development of several types of cancers including breast cancer. This paradoxical identity of E2 undermines the foundations of the physiological definition of “hormone” as E2 works both as a homeostatic regulator of body functions and as a genotoxic compound. Here, (i) the molecular circuitries underlying this double face of E2 are reviewed, and (ii) a possible framework to reconcile the intrinsic discrepancies of the E2 function is reported. Indeed, E2 is a regulator of the DNA damage response, which this hormone exploits to calibrate its genotoxicity with its physiological effects. Accordingly, the genes required to maintain genome integrity belong to the E2-controlled cellular signaling network and are essential for the appearance of the E2-induced cellular effects. This concept requires an “upgrade” to the vision of E2 as a “genotoxic hormone”, which balances physiological and detrimental pathways to guarantee human body homeostasis. Deregulation of this equilibrium between cellular pathways would determine the E2 pathological effects.

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Quantitative mechanisms of DNA damage sensing and signaling

Cited by 11 publications

References 49 publications

Reactive Oxygen Species, Antioxidant Agents, and DNA Damage in Developing Maize Mitochondria and Plastids

Reactive Oxygen Species, Antioxidant Agents, and DNA Damage in Developing Maize Mitochondria and Plastids

Mutant MEG3 Enhances the Activity of Telomerase by Increasing DNA Damage Repair in Human Liver Cancer Stem Cells

A Tale of Ice and Fire: The Dual Role for 17β-Estradiol in Balancing DNA Damage and Genome Integrity

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