Comparative studies of chloroplastic and nuclear DNA repair abilities after ultraviolet irradiation of Euglena gracilis

1980 ◽  
Vol 178 (3) ◽  
pp. 567-572 ◽  
Author(s):  
Paul Nicolas ◽  
Younis Hussein ◽  
Philippe Heizmann ◽  
Victor Nigon
Keyword(s):  
Dna Repair ◽  
Ultraviolet Irradiation ◽  
Euglena Gracilis ◽  
Comparative Studies ◽  
Nuclear Dna

scholarly journals NME3 Regulates Mitochondria to Reduce ROS-Mediated Genome Instability

2020 ◽  
Vol 21 (14) ◽  
pp. 5048
Author(s):  
Chih-Wei Chen ◽  
Ning Tsao ◽  
Wei Zhang ◽  
Zee-Fen Chang
Keyword(s):  
Oxidative Stress ◽  
Dna Repair ◽  
Genome Stability ◽  
Nuclear Dna ◽  
Genome Instability ◽  
Mitochondrial Fission ◽  
Nucleoside Diphosphate Kinase ◽  
Mitochondrial Fusion ◽  
Mitochondrial Outer Membrane ◽  
Mitochondrial Oxidative Stress

NME3 is a member of the nucleoside diphosphate kinase (NDPK) family that binds to the mitochondrial outer membrane to stimulate mitochondrial fusion. In this study, we showed that NME3 knockdown delayed DNA repair without reducing the cellular levels of nucleotide triphosphates. Further analyses revealed that NME3 knockdown increased fragmentation of mitochondria, which in turn led to mitochondrial oxidative stress-mediated DNA single-strand breaks (SSBs) in nuclear DNA. Re-expression of wild-type NME3 or inhibition of mitochondrial fission markedly reduced SSBs and facilitated DNA repair in NME3 knockdown cells, while expression of N-terminal deleted mutant defective in mitochondrial binding had no rescue effect. We further showed that disruption of mitochondrial fusion by knockdown of NME4 or MFN1 also caused mitochondrial oxidative stress-mediated genome instability. In conclusion, the contribution of NME3 to redox-regulated genome stability lies in its function in mitochondrial fusion.

Ultrastructural Changes in Euglena After Ultraviolet Irradiation

1973 ◽  
Vol 13 (3) ◽  
pp. 799-809
Author(s):  
A. MICHAELS ◽  
A. GIBOR
Keyword(s):  
Ultraviolet Light ◽  
Ultraviolet Irradiation ◽  
Euglena Gracilis ◽  
Structural Changes ◽  
Ultrastructural Changes ◽  
Electron Microscopic ◽  
Bleaching Process ◽  
In Cells

The structural changes associated with the ultraviolet-induced bleaching of light-grown cells of Euglena gracilis were investigated. Our light- and electron-microscopic observations of the bleaching process indicate that there is a continuity of plastid structure in cells 5 generations after receiving a bleaching dose of ultraviolet light. There seems to be a continuous dilution of the plastid thylakoids and a decrease in plastid size in the bleaching cells. There also seems to be a change in the position of the plastids in relation to the mitochondria in the bleaching cells. The plastids and possibly the mitochondria are the only organelles which are affected by the ultraviolet irradiation. The continuity of plastids in bleaching cells of Euglena is discussed in relation to the proposed effect of the ultraviolet light.

scholarly journals The mitochondrial outer-membrane location of the EXD2 exonuclease contradicts its direct role in nuclear DNA repair

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Fenna Hensen ◽  
Amandine Moretton ◽  
Selma van Esveld ◽  
Géraldine Farge ◽  
Johannes N. Spelbrink
Keyword(s):  
Dna Repair ◽  
Outer Membrane ◽  
Nuclear Dna ◽  
Mitochondrial Outer Membrane ◽  
Direct Role ◽  
Membrane Location

Age-related decrease in an early step of DNA-repair of normal human lymphocytes exposed to ultraviolet-irradiation

1989 ◽  
Vol 180 (1) ◽  
pp. 171-177 ◽  
Author(s):  
M. Roth ◽  
L.R. Emmons ◽  
M. Häner ◽  
Hj. Müller ◽  
J.M. Boyle
Keyword(s):  
Dna Repair ◽  
Ultraviolet Irradiation ◽  
Human Lymphocytes ◽  
Early Step ◽  
Age Related ◽  
Normal Human

scholarly journals Mechanistic and genetic basis of single-strand templated repair at Cas12a-induced DNA breaks in Chlamydomonas reinhardtii

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Aron Ferenczi ◽  
Yen Peng Chew ◽  
Erika Kroll ◽  
Charlotte von Koppenfels ◽  
Andrew Hudson ◽  
...  
Keyword(s):  
Dna Repair ◽  
Chlamydomonas Reinhardtii ◽  
Nuclear Dna ◽  
Model Organism ◽  
Single Strand ◽  
Dna Double Strand Breaks ◽  
Dna Breaks ◽  
End Joining ◽  
Non Homologous End Joining ◽  
Underlying Mechanisms

AbstractSingle-stranded oligodeoxynucleotides (ssODNs) are widely used as DNA repair templates in CRISPR/Cas precision genome editing. However, the underlying mechanisms of single-strand templated DNA repair (SSTR) are inadequately understood, constraining rational improvements to precision editing. Here we study SSTR at CRISPR/Cas12a-induced DNA double-strand breaks (DSBs) in the eukaryotic model green microalga Chlamydomonas reinhardtii. We demonstrate that ssODNs physically incorporate into the genome during SSTR at Cas12a-induced DSBs. This process is genetically independent of the Rad51-dependent homologous recombination and Fanconi anemia pathways, is strongly antagonized by non-homologous end-joining, and is mediated almost entirely by the alternative end-joining enzyme polymerase θ. These findings suggest differences in SSTR between C. reinhardtii and animals. Our work illustrates the promising potentially of C. reinhardtii as a model organism for studying nuclear DNA repair.

scholarly journals Genome instability is a consequence of transcription deficiency in patients with bone marrow failure harboring biallelic ERCC6L2 variants

2018 ◽  
Vol 115 (30) ◽  
pp. 7777-7782 ◽  
Author(s):  
Hemanth Tummala ◽  
Arran D. Dokal ◽  
Amanda Walne ◽  
Alicia Ellison ◽  
Shirleny Cardoso ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dna Repair ◽  
Rna Polymerase Ii ◽  
Nuclear Dna ◽  
Genome Instability ◽  
Excision Repair ◽  
Bone Marrow Failure ◽  
Rna Pol Ii ◽  
Pol Ii ◽  
Repair Defect

Biallelic variants in the ERCC excision repair 6 like 2 gene (ERCC6L2) are known to cause bone marrow failure (BMF) due to defects in DNA repair and mitochondrial function. Here, we report on eight cases of BMF from five families harboring biallelic variants in ERCC6L2, two of whom present with myelodysplasia. We confirm that ERCC6L2 patients’ lymphoblastoid cell lines (LCLs) are hypersensitive to DNA-damaging agents that specifically activate the transcription coupled nucleotide excision repair (TCNER) pathway. Interestingly, patients’ LCLs are also hypersensitive to transcription inhibitors that interfere with RNA polymerase II (RNA Pol II) and display an abnormal delay in transcription recovery. Using affinity-based mass spectrometry we found that ERCC6L2 interacts with DNA-dependent protein kinase (DNA-PK), a regulatory component of the RNA Pol II transcription complex. Chromatin immunoprecipitation PCR studies revealed ERCC6L2 occupancy on gene bodies along with RNA Pol II and DNA-PK. Patients’ LCLs fail to terminate transcript elongation accurately upon DNA damage and display a significant increase in nuclear DNA–RNA hybrids (R loops). Collectively, we conclude that ERCC6L2 is involved in regulating RNA Pol II-mediated transcription via its interaction with DNA-PK to resolve R loops and minimize transcription-associated genome instability. The inherited BMF syndrome caused by biallelic variants in ERCC6L2 can be considered as a primary transcription deficiency rather than a DNA repair defect.

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