Regulation mechanism of chromatin structure in the maintenance of plant genome stability

2020 ◽  
Vol 32 (1) ◽  
pp. 83-90
Author(s):  
Takeshi Hirakawa
Keyword(s):  
Chromatin Structure ◽  
Genome Stability ◽  
Plant Genome ◽  
Regulation Mechanism

Perfecting DNA double-strand break repair on transcribed chromatin

2020 ◽  
Vol 64 (5) ◽  
pp. 705-719 ◽  
Author(s):  
Xin Yi Tan ◽  
Michael S.Y. Huen
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Chromosomal Aberrations ◽  
Chromatin Structure ◽  
Genome Stability ◽  
Transcriptional Control ◽  
Strand Break ◽  
Double Strand Break ◽  
Dna Double Strand Break ◽  
Molecular Bases

Abstract Timely repair of DNA double-strand break (DSB) entails coordination with the local higher order chromatin structure and its transaction activities, including transcription. Recent studies are uncovering how DSBs trigger transient suppression of nearby transcription to permit faithful DNA repair, failing of which leads to elevated chromosomal aberrations and cell hypersensitivity to DNA damage. Here, we summarize the molecular bases for transcriptional control during DSB metabolism, and discuss how the exquisite coordination between the two DNA-templated processes may underlie maintenance of genome stability and cell homeostasis.

Plant genome stability—General mechanisms

2021 ◽  
pp. 201-222
Author(s):  
Andriy Bilichak ◽  
Narendra Singh Yadav
Keyword(s):  
Genome Stability ◽  
Plant Genome

scholarly journals DNA repair goes hip-hop: SMARCA and CHD chromatin remodellers join the break dance

2017 ◽  
Vol 372 (1731) ◽  
pp. 20160285 ◽  
Author(s):  
Magdalena B. Rother ◽  
Haico van Attikum
Keyword(s):  
Dna Repair ◽  
Posttranslational Modifications ◽  
Chromatin Structure ◽  
Hip Hop ◽  
Genome Stability ◽  
Genome Instability ◽  
Current Knowledge ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks

Proper signalling and repair of DNA double-strand breaks (DSB) is critical to prevent genome instability and diseases such as cancer. The packaging of DNA into chromatin, however, has evolved as a mere obstacle to these DSB responses. Posttranslational modifications and ATP-dependent chromatin remodelling help to overcome this barrier by modulating nucleosome structures and allow signalling and repair machineries access to DSBs in chromatin. Here we recap our current knowledge on how ATP-dependent SMARCA- and CHD-type chromatin remodellers alter chromatin structure during the signalling and repair of DSBs and discuss how their dysfunction impacts genome stability and human disease. This article is part of the themed issue ‘Chromatin modifiers and remodellers in DNA repair and signalling’.

scholarly journals Epigenetic rewriting at centromeric DNA repeats leads to increased chromatin accessibility and chromosomal instability

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Sheldon Decombe ◽  
François Loll ◽  
Laura Caccianini ◽  
Kévin Affannoukoué ◽  
Ignacio Izeddin ◽  
...  
Keyword(s):  
Chromatin Structure ◽  
Genome Stability ◽  
Chromatin Accessibility ◽  
Chromosome 7 ◽  
Epigenetic Mark ◽  
Dna Repeats ◽  
Direct Role ◽  
Artificial Chromosomes ◽  
Natural Context

Abstract Background Centromeric regions of human chromosomes contain large numbers of tandemly repeated α-satellite sequences. These sequences are covered with constitutive heterochromatin which is enriched in trimethylation of histone H3 on lysine 9 (H3K9me3). Although well studied using artificial chromosomes and global perturbations, the contribution of this epigenetic mark to chromatin structure and genome stability remains poorly known in a more natural context. Results Using transcriptional activator-like effectors (TALEs) fused to a histone lysine demethylase (KDM4B), we were able to reduce the level of H3K9me3 on the α-satellites repeats of human chromosome 7. We show that the removal of H3K9me3 affects chromatin structure by increasing the accessibility of DNA repeats to the TALE protein. Tethering TALE-demethylase to centromeric repeats impairs the recruitment of HP1α and proteins of Chromosomal Passenger Complex (CPC) on this specific centromere without affecting CENP-A loading. Finally, the epigenetic re-writing by the TALE-KDM4B affects specifically the stability of chromosome 7 upon mitosis, highlighting the importance of H3K9me3 in centromere integrity and chromosome stability, mediated by the recruitment of HP1α and the CPC. Conclusion Our cellular model allows to demonstrate the direct role of pericentromeric H3K9me3 epigenetic mark on centromere integrity and function in a natural context and opens interesting possibilities for further studies regarding the role of the H3K9me3 mark.

scholarly journals Editorial: MicroRNA Signatures in Plant Genome Stability and Genotoxic Stress

2021 ◽  
Vol 12 ◽  
Author(s):  
Anca Macovei ◽  
Ignacio Rubio-Somoza ◽  
Jorge Almiro Pinto Paiva ◽  
Susana Araújo ◽  
Mattia Donà
Keyword(s):  
Genome Stability ◽  
Genotoxic Stress ◽  
Plant Genome

scholarly journals The Diversity of Plant Small RNAs Silencing Mechanisms

2019 ◽  
Vol 73 (5) ◽  
pp. 362-367 ◽  
Author(s):  
Jens A. Schröder ◽  
Pauline E. Jullien
Keyword(s):  
Gene Regulation ◽  
Gene Silencing ◽  
Small Rna ◽  
Small Rnas ◽  
Genome Stability ◽  
Molecular Mechanisms ◽  
Transcriptional Gene Silencing ◽  
Regulation Mechanism ◽  
Regulatory Processes ◽  
Post Transcriptional Gene Silencing

Small RNAs gene regulation was first discovered about 20 years ago. It represents a conserve gene regulation mechanism across eukaryotes and is associated to key regulatory processes. In plants, small RNAs tightly regulate development, but also maintain genome stability and protect the plant against pathogens. Small RNA gene regulation in plants can be divided in two canonical pathways: Post-transcriptional Gene Silencing (PTGS) that results in transcript degradation and/or translational inhibition or Transcriptional Gene Silencing (TGS) that results in DNA methylation. In this review, we will focus on the model plant Arabidopsis thaliana. We will provide a brief overview of the molecular mechanisms involved in canonical small RNA pathways as well as introducing more atypical pathways recently discovered.

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