Recombinational DNA repair is regulated by compartmentalization of DNA lesions at the nuclear pore complex

Vincent Géli; Michael Lisby

doi:10.1002/bies.201500084

Recombinational DNA repair is regulated by compartmentalization of DNA lesions at the nuclear pore complex

Vincent Géli, Michael Lisby^*

^*Corresponding author for this work

Functional Genomics

25 Citations (Scopus)

Abstract

The nuclear pore complex (NPC) is emerging as a center for recruitment of a class of "difficult to repair" lesions such as double-strand breaks without a repair template and eroded telomeres in telomerase-deficient cells. In addition to such pathological situations, a recent study by Su and colleagues shows that also physiological threats to genome integrity such as DNA secondary structure-forming triplet repeat sequences relocalize to the NPC during DNA replication. Mutants that fail to reposition the triplet repeat locus to the NPC cause repeat instability. Here, we review the types of DNA lesions that relocalize to the NPC, the putative mechanisms of relocalization, and the types of recombinational repair that are stimulated by the NPC, and present a model for NPC-facilitated repair.

Original language	English
Journal	BioEssays
Volume	37
Issue number	12
Pages (from-to)	1287-1292
Number of pages	6
ISSN	0265-9247
DOIs	https://doi.org/10.1002/bies.201500084
Publication status	Published - 2015

Keywords

DNA repair
Homologous recombination
Nuclear organization
Nuclear pore complex
Sumoylation

Access to Document

10.1002/bies.201500084

Cite this

@article{2f089d15f3074cbfaf8d54159782c381,

title = "Recombinational DNA repair is regulated by compartmentalization of DNA lesions at the nuclear pore complex",

abstract = "The nuclear pore complex (NPC) is emerging as a center for recruitment of a class of {"}difficult to repair{"} lesions such as double-strand breaks without a repair template and eroded telomeres in telomerase-deficient cells. In addition to such pathological situations, a recent study by Su and colleagues shows that also physiological threats to genome integrity such as DNA secondary structure-forming triplet repeat sequences relocalize to the NPC during DNA replication. Mutants that fail to reposition the triplet repeat locus to the NPC cause repeat instability. Here, we review the types of DNA lesions that relocalize to the NPC, the putative mechanisms of relocalization, and the types of recombinational repair that are stimulated by the NPC, and present a model for NPC-facilitated repair.",

keywords = "DNA repair, Homologous recombination, Nuclear organization, Nuclear pore complex, Sumoylation",

author = "Vincent G{\'e}li and Michael Lisby",

year = "2015",

doi = "10.1002/bies.201500084",

language = "English",

volume = "37",

pages = "1287--1292",

journal = "BioEssays",

issn = "0265-9247",

publisher = "Wiley",

number = "12",

}

TY - JOUR

T1 - Recombinational DNA repair is regulated by compartmentalization of DNA lesions at the nuclear pore complex

AU - Géli, Vincent

AU - Lisby, Michael

PY - 2015

Y1 - 2015

N2 - The nuclear pore complex (NPC) is emerging as a center for recruitment of a class of "difficult to repair" lesions such as double-strand breaks without a repair template and eroded telomeres in telomerase-deficient cells. In addition to such pathological situations, a recent study by Su and colleagues shows that also physiological threats to genome integrity such as DNA secondary structure-forming triplet repeat sequences relocalize to the NPC during DNA replication. Mutants that fail to reposition the triplet repeat locus to the NPC cause repeat instability. Here, we review the types of DNA lesions that relocalize to the NPC, the putative mechanisms of relocalization, and the types of recombinational repair that are stimulated by the NPC, and present a model for NPC-facilitated repair.

AB - The nuclear pore complex (NPC) is emerging as a center for recruitment of a class of "difficult to repair" lesions such as double-strand breaks without a repair template and eroded telomeres in telomerase-deficient cells. In addition to such pathological situations, a recent study by Su and colleagues shows that also physiological threats to genome integrity such as DNA secondary structure-forming triplet repeat sequences relocalize to the NPC during DNA replication. Mutants that fail to reposition the triplet repeat locus to the NPC cause repeat instability. Here, we review the types of DNA lesions that relocalize to the NPC, the putative mechanisms of relocalization, and the types of recombinational repair that are stimulated by the NPC, and present a model for NPC-facilitated repair.

KW - DNA repair

KW - Homologous recombination

KW - Nuclear organization

KW - Nuclear pore complex

KW - Sumoylation

U2 - 10.1002/bies.201500084

DO - 10.1002/bies.201500084

M3 - Journal article

C2 - 26422820

AN - SCOPUS:84947492342

SN - 0265-9247

VL - 37

SP - 1287

EP - 1292

JO - BioEssays

JF - BioEssays

IS - 12

ER -

Recombinational DNA repair is regulated by compartmentalization of DNA lesions at the nuclear pore complex

Abstract

Keywords

Access to Document

Fingerprint

Cite this