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 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.

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 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 Mutations in RAD27 define a potential link between G1 cyclins and DNA replication.

1995 ◽  
Vol 15 (8) ◽  
pp. 4291-4302 ◽  
Author(s):  
E A Vallen ◽  
F R Cross
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Replication ◽  
Cell Cycle Progression ◽  
Spontaneous Mutation ◽  
Chromosome Loss ◽  
Recombination Rates ◽  
Gene Encoding ◽  
Yeast Saccharomyces Cerevisiae ◽  
Increased Sensitivity

The yeast Saccharomyces cerevisiae has three G1 cyclin (CLN) genes with overlapping functions. To analyze the functions of the various CLN genes, we examined mutations that result in lethality in conjunction with loss of cln1 and cln2. We have isolated alleles of RAD27/ERC11/YKL510, the yeast homolog of the gene encoding flap endonuclease 1, FEN-1.cln1 cln2 rad27/erc11 cells arrest in S phase; this cell cycle arrest is suppressed by the expression of CLN1 or CLN2 but not by that of CLN3 or the hyperactive CLN3-2. rad27/erc11 mutants are also defective in DNA damage repair, as determined by their increased sensitivity to a DNA-damaging agent, increased mitotic recombination rates, and increased spontaneous mutation rates. Unlike the block in cell cycle progression, these phenotypes are not suppressed by CLN1 or CLN2. CLN1 and CLN2 may activate an RAD27/ERC11-independent pathway specific for DNA synthesis that CLN3 is incapable of activating. Alternatively, CLN1 and CLN2 may be capable of overriding a checkpoint response which otherwise causes cln1 cln2 rad27/erc11 cells to arrest. These results imply that CLN1 and CLN2 have a role in the regulation of DNA replication. Consistent with this, GAL-CLN1 expression in checkpoint-deficient, mec1-1 mutant cells results in both cell death and increased chromosome loss among survivors, suggesting that CLN1 overexpression either activates defective DNA replication or leads to insensitivity to DNA damage.

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 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.

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