ArticleMutation research2009
TREX2 exonuclease defective cells exhibit double-strand breaks and chromosomal fragments but not Robertsonian translocations.
Article in Mutation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- NSUN2 is a glucose sensor suppressing cGAS/STING to maintain tumorigenesis and immunotherapy resistance.Cell metabolism · 2023Article
- Exonucleases: Degrading DNA to Deal with Genome Damage, Cell Death, Inflammation and Cancer.Cells · 2022Review
- TREX2 Exonuclease Causes Spontaneous Mutations and Stress-Induced Replication Fork Defects in Cells Expressing RAD51Cell reports · 2020Article
- DNA methylation at an enhancer of the three prime repair exonuclease 2 gene (TREX2) is linked to gene expression and survival in laryngeal cancer.Clinical epigenetics · 2019Article
- Structural insights into the duplex DNA processing of TREX2.Nucleic acids research · 2018Article
- Multifaceted role of TREX2 in the skin defense against UV-induced skin carcinogenesis.Oncotarget · 2015Article
- Neuropathology and genetics of cerebroretinal vasculopathies.Brain pathology (Zurich, Switzerland) · 2014Review
- Two replication fork maintenance pathways fuse inverted repeats to rearrange chromosomes.Nature · 2013Article
- Trex2 enables spontaneous sister chromatid exchanges without facilitating DNA double-strand break repair.Genetics · 2011Article
- One-step knockin for inducible expression in mouse embryonic stem cells.Genesis (New York, N.Y. : 2000) · 2011Article
- Limiting the persistence of a chromosome break diminishes its mutagenic potential.PLoS genetics · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
TREX2 is a 3'-->5' exonuclease that binds to DNA and removes 3' mismatched nucleotides. By an in vitro structure function analysis, we found a single amino acid change (H188A) completely ablates exonuclease activity and impairs DNA binding by about 60% while another change (R167A) impairs DNA binding by about 85% without impacting exonuclease activity. For a biological analysis, we generated trex2null cells by deleting the entire Trex2 coding sequences in mouse embryonic stem (ES) cells. We found Trex2 deletion caused high levels of Robertsonian translocations (RbTs) showing Trex2 is important for chromosomal maintenance. Here we evaluate the exonuclease and DNA binding domains by expressing in trex2(null) cells coding sequences for wild type human TREX2 (Trex2hTX2) or human TREX2 with the H188A change (Trex2H188A) or the R167A change (Trex2R167A). These cDNAs are positioned adjacent to the mouse Trex2 promoter by Cre-mediated knock-in. By observing metaphase spreads, we found Trex2H188A cells exhibited high levels of double-strand breaks (DSBs) and chromosomal fragments. Therefore, TREX2 may suppress spontaneous DSBs or exonuclease defective TREX2 may induce them in a dominate-negative manner. We also found Trex2hTX2, hTrex2H188A and hTrex2R167A cells did not exhibit RbTs. Thus, neither the exonuclease nor DNA binding domains suppress RbTs suggesting TREX2 possesses additional biochemical activities.
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