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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Cell+Biol
2016 ; 215
(6
): 801-821
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LINC complexes promote homologous recombination in part through inhibition of
nonhomologous end joining
#MMPMID27956467
Lawrence KS
; Tapley EC
; Cruz VE
; Li Q
; Aung K
; Hart KC
; Schwartz TU
; Starr DA
; Engebrecht J
J Cell Biol
2016[Dec]; 215
(6
): 801-821
PMID27956467
show ga
The Caenorhabditis elegans SUN domain protein, UNC-84, functions in nuclear
migration and anchorage in the soma. We discovered a novel role for UNC-84 in DNA
damage repair and meiotic recombination. Loss of UNC-84 leads to defects in the
loading and disassembly of the recombinase RAD-51. Similar to mutations in
Fanconi anemia (FA) genes, unc-84 mutants and human cells depleted of Sun-1 are
sensitive to DNA cross-linking agents, and sensitivity is rescued by the
inactivation of nonhomologous end joining (NHEJ). UNC-84 also recruits FA
nuclease FAN-1 to the nucleoplasm, suggesting that UNC-84 both alters the extent
of repair by NHEJ and promotes the processing of cross-links by FAN-1. UNC-84
interacts with the KASH protein ZYG-12 for DNA damage repair. Furthermore, the
microtubule network and interaction with the nucleoskeleton are important for
repair, suggesting that a functional linker of nucleoskeleton and cytoskeleton
(LINC) complex is required. We propose that LINC complexes serve a conserved role
in DNA repair through both the inhibition of NHEJ and the promotion of homologous
recombination at sites of chromosomal breaks.