ArticleGenetics2011
Trex2 enables spontaneous sister chromatid exchanges without facilitating DNA double-strand break repair.
Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Super-resolution visualization and modeling of human chromosomal regions reveals cohesin-dependent loop structures.Genome biology · 2021Article
- TREX2 Exonuclease Causes Spontaneous Mutations and Stress-Induced Replication Fork Defects in Cells Expressing RAD51Cell reports · 2020Article
- Methods Favoring Homology-Directed Repair Choice in Response to CRISPR/Cas9 Induced-Double Strand Breaks.International journal of molecular sciences · 2020Review
- Structural insights into the duplex DNA processing of TREX2.Nucleic acids research · 2018Article
- A mechanism for 1,4-Benzoquinone-induced genotoxicity.Oncotarget · 2016Article
- Chromosomal Rearrangements in Cancer: Detection and potential causal mechanisms.Molecular & cellular oncology · 2014Article
- Two replication fork maintenance pathways fuse inverted repeats to rearrange chromosomes.Nature · 2013Article
- Defining a genotoxic profile with mouse embryonic stem cells.Experimental biology and medicine (Maywood, N.J.) · 2013Review
- RAD51 mutants cause replication defects and chromosomal instability.Molecular and cellular biology · 2012Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Trex2 is a 3' → 5' exonuclease that removes 3'-mismatched sequences in a biochemical assay; however, its biological function remains unclear. To address biology we previously generated trex2(null) mouse embryonic stem (ES) cells and expressed in these cells wild-type human TREX2 cDNA (Trex2(hTX2)) or cDNA with a single-amino-acid change in the catalytic domain (Trex2(H188A)) or in the DNA-binding domain (Trex2(R167A)). We found the trex2(null) and Trex2(H188A) cells exhibited spontaneous broken chromosomes and trex2(null) cells exhibited spontaneous chromosomal rearrangements. We also found ectopically expressed human TREX2 was active at the 3' ends of I-SceI-induced chromosomal double-strand breaks (DSBs). Therefore, we hypothesized Trex2 participates in DNA DSB repair by modifying 3' ends. This may be especially important for ends with damaged nucleotides. Here we present data that are unexpected and prompt a new model. We found Trex2-altered cells (null, H188A, and R167A) were not hypersensitive to camptothecin, a type-1 topoisomerase inhibitor that induces DSBs at replication forks. In addition, Trex2-altered cells were not hypersensitive to γ-radiation, an agent that causes DSBs throughout the cell cycle. This observation held true even in cells compromised for one of the two major DSB repair pathways: homology-directed repair (HDR) or nonhomologous end joining (NHEJ). Trex2 deletion also enhanced repair of an I-SceI-induced DSB by both HDR and NHEJ without affecting pathway choice. Interestingly, however, trex2(null) cells exhibited reduced spontaneous sister chromatid exchanges (SCEs) but this was not due to a defect in HDR-mediated crossing over. Therefore, reduced spontaneous SCE could be a manifestation of the same defect that caused spontaneous broken chromosomes and spontaneous chromosomal rearrangements. These unexpected data suggest Trex2 does not enable DSB repair and prompt a new model that posits Trex2 suppresses the formation of broken chromosomes.
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