scholarly journals Methods to Study the Atypical Roles of DNA Repair and SMC Proteins in Gene Silencing

2016 ◽  
pp. 151-176
Author(s):  
Misty R. Peterson ◽  
Omar Hamdani ◽  
Rohinton T. Kamakaka
Keyword(s):  
Dna Repair ◽  
Gene Silencing ◽  
Smc Proteins

scholarly journals Gene silencing in phenomena related to DNA repair

Oncogene ◽  
2002 ◽  
Vol 21 (58) ◽  
pp. 9033-9042 ◽  
Author(s):  
Tsunehiro Mukai ◽  
Mutsuo Sekiguchi
Keyword(s):  
Dna Repair ◽  
Gene Silencing

scholarly journals Crystal structure of the ATPase-C domain of the chromatin remodeller Fun30 fromSaccharomyces cerevisiae

2017 ◽  
Vol 73 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Lan Liu ◽  
Tao Jiang
Keyword(s):  
Crystal Structure ◽  
Dna Repair ◽  
Gene Silencing ◽  
Chromatin Structure ◽  
Family Members ◽  
Atpase Domain ◽  
Repair Gene ◽  
Dna Repair Gene

Fun30 (Function unknown now 30) is a chromatin remodeller belonging to the Snf2 family. It has previously been reported to be a regulator of several cellular activities, including DNA repair, gene silencing and maintenance of chromatin structure. Here, the crystal structure of the Fun30 ATPase-C domain (the C-lobe of the ATPase domain) is reported at 1.95 Å resolution. Although the structure displays overall similarities to those of other Snf2 family members, a new structural module was found to be specific to the Fun30 subfamily. Fun30 ATPase-C was shown be monomeric in solution and showed no detectable affinity for dsDNA.

scholarly journals Screen identifies DYRK1B network as mediator of transcription repression on damaged chromatin

2020 ◽  
Vol 117 (29) ◽  
pp. 17019-17030 ◽  
Author(s):  
Chao Dong ◽  
Kirk L. West ◽  
Xin Yi Tan ◽  
Junshi Li ◽  
Toyotaka Ishibashi ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Gene Silencing ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Active Chromatin ◽  
Chemical Library ◽  
Dsb Repair ◽  
Strand Breaks ◽  
Damage Response

DNA double-strand breaks (DSBs) trigger transient pausing of nearby transcription, an emerging ATM-dependent response that suppresses chromosomal instability. We screened a chemical library designed to target the human kinome for new activities that mediate gene silencing on DSB-flanking chromatin, and have uncovered the DYRK1B kinase as an early respondent to DNA damage. We showed that DYRK1B is swiftly and transiently recruited to laser-microirradiated sites, and that genetic inactivation of DYRK1B or its kinase activity attenuated DSB-induced gene silencing and led to compromised DNA repair. Notably, global transcription shutdown alleviated DNA repair defects associated with DYRK1B loss, suggesting that DYRK1B is strictly required for DSB repair on active chromatin. We also found that DYRK1B mediates transcription silencing in part via phosphorylating and enforcing DSB accumulation of the histone methyltransferase EHMT2. Together, our findings unveil the DYRK1B signaling network as a key branch of mammalian DNA damage response circuitries, and establish the DYRK1B–EHMT2 axis as an effector that coordinates DSB repair on transcribed chromatin.

scholarly journals Concatenation of Transgenic DNA: Random or Orchestrated?

Genes ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1969
Author(s):  
Alexander Smirnov ◽  
Nariman Battulin
Keyword(s):  
Dna Repair ◽  
Gene Silencing ◽  
Tandem Repeats ◽  
Routine Procedure ◽  
Dna Integration ◽  
Pronuclear Microinjection ◽  
Transgenic Organisms ◽  
Dna Injection ◽  
Repair Pathways

Generation of transgenic organisms by pronuclear microinjection has become a routine procedure. However, while the process of DNA integration in the genome is well understood, we still do not know much about the recombination between transgene molecules that happens in the first moments after DNA injection. Most of the time, injected molecules are joined together in head-to-tail tandem repeats—the so-called concatemers. In this review, we focused on the possible concatenation mechanisms and how they could be studied with genetic reporters tracking individual copies in concatemers. We also discuss various features of concatemers, including palindromic junctions and repeat-induced gene silencing (RIGS). Finally, we speculate how cooperation of DNA repair pathways creates a multicopy concatenated insert.

scholarly journals Purkinje Cell Degeneration inpcdMice Reveals Large Scale Chromatin Reorganization and Gene Silencing Linked to Defective DNA Repair

2011 ◽  
Vol 286 (32) ◽  
pp. 28287-28302 ◽  
Author(s):  
Fernando C. Baltanás ◽  
Iñigo Casafont ◽  
Vanesa Lafarga ◽  
Eduardo Weruaga ◽  
José R. Alonso ◽  
...  
Keyword(s):  
Dna Repair ◽  
Purkinje Cell ◽  
Gene Silencing ◽  
Large Scale ◽  
Cell Degeneration ◽  
Purkinje Cell Degeneration ◽  
Defective Dna Repair ◽  
Chromatin Reorganization

scholarly journals The Role of Polycomb Group Protein BMI1 in DNA Repair and Genomic Stability

2021 ◽  
Vol 22 (6) ◽  
pp. 2976
Author(s):  
Amira Fitieh ◽  
Andrew J. Locke ◽  
Mobina Motamedi ◽  
Ismail Hassan Ismail
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Gene Silencing ◽  
Strand Break ◽  
Polycomb Group ◽  
Polycomb Group Protein ◽  
Post Translational Modifications ◽  
Dna Damage Signaling ◽  
Dna Double Strand Break ◽  
Group Protein

The polycomb group (PcG) proteins are a class of transcriptional repressors that mediate gene silencing through histone post-translational modifications. They are involved in the maintenance of stem cell self-renewal and proliferation, processes that are often dysregulated in cancer. Apart from their canonical functions in epigenetic gene silencing, several studies have uncovered a function for PcG proteins in DNA damage signaling and repair. In particular, members of the poly-comb group complexes (PRC) 1 and 2 have been shown to recruit to sites of DNA damage and mediate DNA double-strand break repair. Here, we review current understanding of the PRCs and their roles in cancer development. We then focus on the PRC1 member BMI1, discussing the current state of knowledge of its role in DNA repair and genome integrity, and outline how it can be targeted pharmacologically.

scholarly journals Arabidopsis RPA2: A Genetic Link among Transcriptional Gene Silencing, DNA Repair, and DNA Replication

2005 ◽  
Vol 15 (21) ◽  
pp. 1919-1925 ◽  
Author(s):  
Taline Elmayan ◽  
Florence Proux ◽  
Hervé Vaucheret
Keyword(s):  
Dna Repair ◽  
Dna Replication ◽  
Gene Silencing ◽  
Transcriptional Gene Silencing ◽  
Genetic Link

scholarly journals Role of Saccharomyces cerevisiae Chromatin Assembly Factor-I in Repair of Ultraviolet Radiation Damage in Vivo

Genetics ◽  
1999 ◽  
Vol 151 (2) ◽  
pp. 485-497 ◽  
Author(s):  
John C Game ◽  
Paul D Kaufman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Gene Silencing ◽  
Chromatin Assembly ◽  
Yeast Cells ◽  
Repair Gene ◽  
Uv Sensitivity ◽  
Factor I ◽  
Chromatin Assembly Factor ◽  
Assembly Factor

Abstract In vitro, the protein complex Chromatin Assembly Factor-I (CAF-I) from human or yeast cells deposits histones onto DNA templates after replication. In Saccharomyces cerevisiae, the CAC1, CAC2, and CAC3 genes encode the three CAF-I subunits. Deletion of any of the three CAC genes reduces telomeric gene silencing and confers an increase in sensitivity to killing by ultraviolet (UV) radiation. We used double and triple mutants involving cac1Δ and yeast repair gene mutations to show that deletion of the CAC1 gene increases the UV sensitivity of cells mutant in genes from each of the known DNA repair epistasis groups. For example, double mutants involving cac1Δ and excision repair gene deletions rad1Δ or rad14Δ showed increased UV sensitivity, as did double mutants involving cac1Δ and deletions of members of the RAD51 recombinational repair group. cac1Δ also increased the UV sensitivity of strains with defects in either the error-prone (rev3Δ) or error-free (pol30-46) branches of RAD6-mediated postreplicative DNA repair but did not substantially increase the sensitivity of strains carrying null mutations in the RAD6 or RAD18 genes. Deletion of CAC1 also increased the UV sensitivity and rate of UV-induced mutagenesis in rad5Δ mutants, as has been observed for mutants defective in error-free postreplicative repair. Together, these data suggest that CAF-I has a role in error-free postreplicative damage repair and may also have an auxiliary role in other repair mechanisms. Like the CAC genes, RAD6 is also required for gene silencing at telomeres. We find an increased loss of telomeric gene silencing in rad6Δ cac1Δ and rad18Δ cac1Δ double mutants, suggesting that CAF-I and multiple factors in the postreplicative repair pathway influence chromosome structure.

scholarly journals Heterochromatin formation via recruitment of DNA repair proteins

2015 ◽  
Vol 26 (7) ◽  
pp. 1395-1410 ◽  
Author(s):  
Jacob G. Kirkland ◽  
Misty R. Peterson ◽  
Christopher D. Still ◽  
Leo Brueggeman ◽  
Namrita Dhillon ◽  
...  
Keyword(s):  
Dna Repair ◽  
Gene Silencing ◽  
Nuclear Organization ◽  
Nuclear Periphery ◽  
Strand Break ◽  
Atm Kinase ◽  
Heterochromatin Formation ◽  
Sir Proteins ◽  
Repair Protein ◽  
Dna Repair Proteins

Heterochromatin formation and nuclear organization are important in gene regulation and genome fidelity. Proteins involved in gene silencing localize to sites of damage and some DNA repair proteins localize to heterochromatin, but the biological importance of these correlations remains unclear. In this study, we examined the role of double-strand-break repair proteins in gene silencing and nuclear organization. We find that the ATM kinase Tel1 and the proteins Mre11 and Esc2 can silence a reporter gene dependent on the Sir, as well as on other repair proteins. Furthermore, these proteins aid in the localization of silenced domains to specific compartments in the nucleus. We identify two distinct mechanisms for repair protein–mediated silencing—via direct and indirect interactions with Sir proteins, as well as by tethering loci to the nuclear periphery. This study reveals previously unknown interactions between repair proteins and silencing proteins and suggests insights into the mechanism underlying genome integrity.

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