REXO5 promotes genomic integrity through regulating R-loop using its exonuclease activity.
Ye Jin LeeSeo Yun LeeSoomi KimSoo-Hyun KimSoo Hyeon LeeSungho ParkJae Jin KimDong-Wook KimHongtae KimPublished in: Leukemia (2024)
Chronic myeloid leukemia (CML), caused by BCR::ABL1 fusion gene, is known to regulate disease progression by altering the expression of genes. However, the molecular mechanisms underlying these changes are largely unknown. In this study, we identified RNA Exonuclease 5 (REXO5/LOC81691) as a novel gene with elevated mRNA expression levels in chronic myeloid leukemia (CML) patients. Additionally, using the REXO5 knockout (KO) K562 cell lines, we revealed a novel role for REXO5 in the DNA damage response (DDR). Compared to wild-type (WT) cells, REXO5 KO cells showed an accumulation of R-loops and increased DNA damage. We demonstrated that REXO5 translocates to sites of DNA damage through its RNA recognition motif (RRM) and selectively binds to R loops. Interestingly, we identified that REXO5 regulates R-loop levels by degrading mRNA within R-loop using its exonuclease domain. REXO5 KO showed ATR-CHK1 activation. Collectively, we demonstrated that REXO5 plays a key role in the physiological control of R-loops using its exonuclease domain. These findings may provide novel insights into how REXO5 expression changes contribute to CML pathogenesis.
Keyphrases
- chronic myeloid leukemia
- dna damage response
- dna damage
- induced apoptosis
- dna repair
- poor prognosis
- wild type
- end stage renal disease
- oxidative stress
- genome wide
- cell cycle arrest
- copy number
- transcription factor
- genome wide identification
- chronic kidney disease
- newly diagnosed
- peritoneal dialysis
- cell death
- signaling pathway
- patient reported outcomes
- gene expression
- genome wide analysis
- acute lymphoblastic leukemia
- tyrosine kinase
- long non coding rna