Imaging DNA damage-dependent chromatin dynamics via nonlinear photoperturbation

CLEO: 2013 ◽  
2013 ◽  
Author(s):  
M. Tomas ◽  
P. Blumhardt ◽  
A. Deutzmann ◽  
D. Kromm ◽  
A. Leitenstorfer ◽  
...  
Keyword(s):  
Dna Damage ◽  
Chromatin Dynamics

scholarly journals DNA repair mechanisms and gametogenesis

Reproduction ◽  
2001 ◽  
pp. 31-39 ◽  
Author(s):  
WM Baarends ◽  
R van der Laan ◽  
JA Grootegoed
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Gene Knockout ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Control ◽  
Chromatin Dynamics ◽  
Dna Mismatch ◽  
Dna Repair Mechanisms ◽  
Genes Encoding ◽  
Repair Mechanisms

In mammals, there is a complex and intriguing relationship between DNA repair and gametogenesis. DNA repair mechanisms are involved not only in the repair of different types of DNA damage in developing germline cells, but also take part in the meiotic recombination process. Furthermore, the DNA repair mechanisms should tolerate mutations occurring during gametogenesis, to a limited extent. In the present review, several gametogenic aspects of DNA mismatch repair, homologous recombination repair and postreplication repair are discussed. In addition, the role of DNA damage-induced cell cycle checkpoint control is considered briefly. It appears that many genes encoding proteins that take part in DNA repair mechanisms show enhanced or specialized expression during mammalian gametogenesis, and several gene knockout mouse models show male or female infertility. On the basis of such knowledge and models, future experiments may provide more information about the precise relationship between DNA repair, chromatin dynamics, and genomic stability versus instability during gametogenesis.

scholarly journals Monoubiquitylation of histone H2B contributes to the bypass of DNA damage during and after DNA replication

2017 ◽  
Vol 114 (11) ◽  
pp. E2205-E2214 ◽  
Author(s):  
Shih-Hsun Hung ◽  
Ronald P. Wong ◽  
Helle D. Ulrich ◽  
Cheng-Fu Kao
Keyword(s):  
Dna Damage ◽  
Replication Fork ◽  
Dna Lesions ◽  
Template Switching ◽  
Lesion Bypass ◽  
Dna Damage Tolerance ◽  
Cytological Evidence ◽  
Histone H2b ◽  
Chromatin Dynamics ◽  
Dna Lesion

DNA lesion bypass is mediated by DNA damage tolerance (DDT) pathways and homologous recombination (HR). The DDT pathways, which involve translesion synthesis and template switching (TS), are activated by the ubiquitylation (ub) of PCNA through components of the RAD6-RAD18 pathway, whereas the HR pathway is independent of RAD18. However, it is unclear how these processes are coordinated within the context of chromatin. Here we show that Bre1, an ubiquitin ligase specific for histone H2B, is recruited to chromatin in a manner coupled to replication of damaged DNA. In the absence of Bre1 or H2Bub, cells exhibit accumulation of unrepaired DNA lesions. Consequently, the damaged forks become unstable and resistant to repair. We provide physical, genetic, and cytological evidence that H2Bub contributes toward both Rad18-dependent TS and replication fork repair by HR. Using an inducible system of DNA damage bypass, we further show that H2Bub is required for the regulation of DDT after genome duplication. We propose that Bre1-H2Bub facilitates fork recovery and gap-filling repair by controlling chromatin dynamics in response to replicative DNA damage.

scholarly journals Multi-scale tracking reveals scale-dependent chromatin dynamics after DNA damage

2017 ◽  
Vol 28 (23) ◽  
pp. 3323-3332 ◽  
Author(s):  
Judith Miné-Hattab ◽  
Vincent Recamier ◽  
Ignacio Izeddin ◽  
Rodney Rothstein ◽  
Xavier Darzacq
Keyword(s):  
Dna Damage ◽  
Time Scales ◽  
Persistence Length ◽  
Chromatin Dynamics ◽  
Strand Breaks ◽  
Multi Scale ◽  
Repair Protein ◽  
Global Increase ◽  
Dna Motion ◽  
Short Time

The dynamic organization of genes inside the nucleus is an important determinant for their function. Using fast DNA tracking microscopy in Saccharomyces cerevisiae cells and improved analysis of mean-squared displacements, we quantified DNA motion at time scales ranging from 10 ms to minutes and found that following DNA damage, DNA exhibits distinct subdiffusive regimes. In response to double-strand breaks, chromatin is more mobile at large time scales, but, surprisingly, its mobility is reduced at short time scales. This effect is even more pronounced at the site of damage. Such a pattern of dynamics is consistent with a global increase in chromatin persistence length in response to DNA damage. Scale-dependent nuclear exploration is regulated by the Rad51 repair protein, both at the break and throughout of the genome. We propose a model in which stiffening of the damaged ends by the repair complex, combined with global increased stiffness, act like a “needle in a ball of yarn,” enhancing the ability of the break to traverse the chromatin meshwork.

scholarly journals Chromatin Dynamics in Genome Stability: Roles in Suppressing Endogenous DNA Damage and Facilitating DNA Repair

2017 ◽  
Vol 18 (7) ◽  
pp. 1486 ◽  
Author(s):  
Nidhi Nair ◽  
Muhammad Shoaib ◽  
Claus Storgaard Sørensen
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Genome Stability ◽  
Chromatin Dynamics

scholarly journals Histone degradation in response to DNA damage enhances chromatin dynamics and recombination rates

2017 ◽  
Vol 24 (2) ◽  
pp. 99-107 ◽  
Author(s):  
Michael H Hauer ◽  
Andrew Seeber ◽  
Vijender Singh ◽  
Raphael Thierry ◽  
Ragna Sack ◽  
...  
Keyword(s):  
Dna Damage ◽  
Recombination Rates ◽  
Chromatin Dynamics

scholarly journals Interphase Chromatin Dynamics in Response to Local DNA Damage

2017 ◽  
Vol 112 (3) ◽  
pp. 374a
Author(s):  
Jonah Eaton ◽  
Alexandra Zidovska
Keyword(s):  
Dna Damage ◽  
Interphase Chromatin ◽  
Chromatin Dynamics

scholarly journals Chromatin Dynamics and the Fanconi Anemia DNA Damage Response Pathway

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Karissa L Neira ◽  
Maurizio Mauro ◽  
Niall G Howlett
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Fanconi Anemia ◽  
Chromatin Dynamics ◽  
Damage Response ◽  
Dna Damage Response Pathway

scholarly journals Modified chromosome structure caused by phosphomimetic H2A modulates the DNA damage response by increasing chromatin mobility in yeast

2021 ◽  
Vol 134 (6) ◽  
Author(s):  
Fabiola García Fernández ◽  
Brenda Lemos ◽  
Yasmine Khalil ◽  
Renaud Batrin ◽  
James E. Haber ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Structural Changes ◽  
Sharp Decrease ◽  
Histone H2a ◽  
End Joining ◽  
Chromatin Dynamics ◽  
Damage Response ◽  
Chromatin Structural ◽  
Non Homologous End Joining

ABSTRACT In budding yeast and mammals, double-strand breaks (DSBs) trigger global chromatin mobility together with rapid phosphorylation of histone H2A over an extensive region of the chromatin. To assess the role of H2A phosphorylation in this response to DNA damage, we have constructed strains where H2A has been mutated to the phosphomimetic H2A-S129E. We show that mimicking H2A phosphorylation leads to an increase in global chromatin mobility in the absence of DNA damage. The intrinsic chromatin mobility of H2A-S129E is not due to downstream checkpoint activation, histone degradation or kinetochore anchoring. Rather, the increased intrachromosomal distances observed in the H2A-S129E mutant are consistent with chromatin structural changes. Strikingly, in this context the Rad9-dependent checkpoint becomes dispensable. Moreover, increased chromatin dynamics in the H2A-S129E mutant correlates with improved DSB repair by non-homologous end joining and a sharp decrease in interchromosomal translocation rate. We propose that changes in chromosomal conformation due to H2A phosphorylation are sufficient to modulate the DNA damage response and maintain genome integrity. This article has an associated First Person interview with the first author of the paper.

scholarly journals DNA Damage-Dependent Acetylation and Ubiquitination of H2AX Enhances Chromatin Dynamics

2007 ◽  
Vol 27 (20) ◽  
pp. 7028-7040 ◽  
Author(s):  
Tsuyoshi Ikura ◽  
Satoshi Tashiro ◽  
Akemi Kakino ◽  
Hiroki Shima ◽  
Naduparambil Jacob ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Cell Cycle Checkpoints ◽  
Variant Form ◽  
Ionizing Irradiation ◽  
Chromatin Dynamics ◽  
Histone H2ax ◽  
Damage Response ◽  
Ubiquitin Conjugating Enzyme ◽  
Chromatin Reorganization

ABSTRACT Chromatin reorganization plays an important role in DNA repair, apoptosis, and cell cycle checkpoints. Among proteins involved in chromatin reorganization, TIP60 histone acetyltransferase has been shown to play a role in DNA repair and apoptosis. However, how TIP60 regulates chromatin reorganization in the response of human cells to DNA damage is largely unknown. Here, we show that ionizing irradiation induces TIP60 acetylation of histone H2AX, a variant form of H2A known to be phosphorylated following DNA damage. Furthermore, TIP60 regulates the ubiquitination of H2AX via the ubiquitin-conjugating enzyme UBC13, which is induced by DNA damage. This ubiquitination of H2AX requires its prior acetylation. We also demonstrate that acetylation-dependent ubiquitination by the TIP60-UBC13 complex leads to the release of H2AX from damaged chromatin. We conclude that the sequential acetylation and ubiquitination of H2AX by TIP60-UBC13 promote enhanced histone dynamics, which in turn stimulate a DNA damage response.

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