scholarly journals Telomere tethering at the nuclear periphery is essential for efficient DNA double strand break repair in subtelomeric region

2006 ◽  
Vol 172 (2) ◽  
pp. 189-199 ◽  
Author(s):  
Pierre Therizols ◽  
Cécile Fairhead ◽  
Ghislain G. Cabal ◽  
Auguste Genovesio ◽  
Jean-Christophe Olivo-Marin ◽  
...  
Keyword(s):  
Functional Organization ◽  
Nuclear Periphery ◽  
Strand Break ◽  
Double Strand Break ◽  
Subtelomeric Region ◽  
Genome Integrity ◽  
Nuclear Pore ◽  
Core Complex ◽  
Yeast Saccharomyces Cerevisiae ◽  
Dna Double Strand Break

In the yeast Saccharomyces cerevisiae that lacks lamins, the nuclear pore complex (NPC) has been proposed to serve a role in chromatin organization. Here, using fluorescence microscopy in living cells, we show that nuclear pore proteins of the Nup84 core complex, Nup84p, Nup145Cp, Nup120p, and Nup133p, serve to anchor telomere XI-L at the nuclear periphery. The integrity of this complex is shown to be required for repression of a URA3 gene inserted in the subtelomeric region of this chromosome end. Furthermore, altering the integrity of this complex decreases the efficiency of repair of a DNA double-strand break (DSB) only when it is generated in the subtelomeric region, even though the repair machinery is functional. These effects are specific to the Nup84 complex. Our observations thus confirm and extend the role played by the NPC, through the Nup84 complex, in the functional organization of chromatin. They also indicate that anchoring of telomeres is essential for efficient repair of DSBs occurring therein and is important for preserving genome integrity.

scholarly journals Correction: Telomere tethering at the nuclear periphery is essential for efficient DNA double strand break repair in subtelomeric region

2006 ◽  
Vol 172 (6) ◽  
pp. 951-951
Author(s):  
Pierre Therizols ◽  
Cécile Fairhead ◽  
Ghislain G. Cabal ◽  
Auguste Genovesio ◽  
Jean-Christophe Olivo-Marin ◽  
...  
Keyword(s):  
Nuclear Periphery ◽  
Strand Break ◽  
Double Strand Break ◽  
Subtelomeric Region ◽  
Double Strand Break Repair ◽  
Dna Double Strand Break ◽  
Break Repair

scholarly journals Localisation of Nup153 and SENP1 to nuclear pore complexes is required for 53BP1-mediated DNA double-strand break repair

2017 ◽  
Vol 130 (14) ◽  
pp. 2306-2316 ◽  
Author(s):  
Vincent Duheron ◽  
Nadine Nilles ◽  
Sylvia Pecenko ◽  
Valérie Martinelli ◽  
Birthe Fahrenkrog
Keyword(s):  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Nuclear Pore ◽  
Nuclear Pore Complexes ◽  
Dna Double Strand Break ◽  
Break Repair ◽  
Pore Complexes

scholarly journals DMC1 Functions in a Saccharomyces cerevisiae Meiotic Pathway That Is Largely Independent of the RAD51 Pathway

Genetics ◽  
1997 ◽  
Vol 147 (2) ◽  
pp. 533-544 ◽  
Author(s):  
Michael E Dresser ◽  
Debra J Ewing ◽  
Michael N Conrad ◽  
Ana M Dominguez ◽  
Robert Barstead ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Fusion Proteins ◽  
Strand Break ◽  
Double Strand Break ◽  
Yeast Saccharomyces Cerevisiae ◽  
Atp Binding Site ◽  
Epistasis Analysis ◽  
Dna Double Strand Break ◽  
Chromosome Fragments ◽  
Two Hybrid

Meiotic recombinationin the yeast Saccharomyces cerevisiae requires two similar recA-like proteins, Dmc1p and Rad51p. A screen for dominant meiotic mutants provided DMC1-G126D, a dominant allele mutated in the conserved ATP-binding site (specifically, the A-loop motif) that confers a null phenotype. A recessive null allele, dmc1-K69E, was isolated as an intragenic suppressor of DMC1-G126D. Dmc1-K69Ep, unlike Dmc1p, does not interact homotypically in a two-hybrid assay, although it does interact with other fusion proteins identified by two-hybrid screen with Dmc1p. Dmc1p, unlike Rad51p, does not interact in the two-hybrid assay with Rad52p or Rad54p. However, Dmc1p does interact with Tid1p, a Rad54p homologue, with Tid4p, a Rad16p homologue, and with other fusion proteins that do not interact with Rad51p, suggesting that Dmc1p and Rad51p function in separate, though possibly overlapping, recombinational repair complexes. Epistasis analysis suggests that DMC1 and RAD51 function in separate pathways responsible for meiotic recombination. Taken together, our results are consistent with a requirement for DMC1 for meiosis-specific entry of DNA double-strand break ends into chromatin. Interestingly, the pattern on CHEF gels of chromosome fragments that result from meiotic DNA double-strand break formation is different in DMC1 mutant strains from that seen in rad50S strains.

scholarly journals Mechanisms that regulate localization of a DNA double-strand break to the nuclear periphery

2009 ◽  
Vol 23 (8) ◽  
pp. 912-927 ◽  
Author(s):  
P. Oza ◽  
S. L. Jaspersen ◽  
A. Miele ◽  
J. Dekker ◽  
C. L. Peterson
Keyword(s):  
Nuclear Periphery ◽  
Strand Break ◽  
Double Strand Break ◽  
Dna Double Strand Break

scholarly journals Preserving genome integrity in human cells via DNA double-strand break repair

2020 ◽  
Vol 31 (9) ◽  
pp. 859-865 ◽  
Author(s):  
Ryan B. Jensen ◽  
Eli Rothenberg
Keyword(s):  
Dna Repair ◽  
Strand Break ◽  
Double Strand Break ◽  
Human Cells ◽  
Cell Cycle Checkpoints ◽  
Human Diseases ◽  
Genome Integrity ◽  
Dsb Repair ◽  
Dna Double Strand Break ◽  
Repair Pathways

The efficient maintenance of genome integrity in the face of cellular stress is vital to protect against human diseases such as cancer. DNA replication, chromatin dynamics, cellular signaling, nuclear architecture, cell cycle checkpoints, and other cellular activities contribute to the delicate spatiotemporal control that cells utilize to regulate and maintain genome stability. This perspective will highlight DNA double-strand break (DSB) repair pathways in human cells, how DNA repair failures can lead to human disease, and how PARP inhibitors have emerged as a novel clinical therapy to treat homologous recombination-deficient tumors. We briefly discuss how failures in DNA repair produce a permissive genetic environment in which preneoplastic cells evolve to reach their full tumorigenic potential. Finally, we conclude that an in-depth understanding of DNA DSB repair pathways in human cells will lead to novel therapeutic strategies to treat cancer and potentially other human diseases.

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