Mol Cell | 薛毅博等揭示DDIAS介导有丝分裂期单链DNA的修复
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TL;DR - A Molecular Cell study identifies DDIAS as the ssDNA-binding effector of the CIP2A–TOPBP1 complex, revealing a DNA synthesis-dependent pathway that repairs single-stranded DNA during mitosis. This mechanism helps preserve chromosome integrity and influences PARP-inhibitor sensitivity in BRCA1/2-deficient cells.
- DDIAS binds phosphorylated TOPBP1 through its BRCT7/8 domains and is recruited to mitotic DNA-damage sites.
- DDIAS’s ssDNA-binding activity is required for CIP2A–TOPBP1 function and mitotic genome stability.
- ssDNA accumulated in BRCA1/2-deficient cells during G2—especially after PARP inhibition—is largely removed by prometaphase through a DDIAS- and DNA synthesis-dependent process.
- The findings establish the CIP2A–TOPBP1–DDIAS axis as a mitotic ssDNA-repair system distinct from canonical DNA-damage responses.
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Mol Cell | 薛毅博等揭示DDIAS介导有丝分裂期单链DNA的修复
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TL;DR - A Molecular Cell study identifies DDIAS as the ssDNA-binding effector of the CIP2A–TOPBP1 complex, revealing a DNA synthesis-dependent pathway that repairs single-stranded DNA during mitosis. This mechanism helps preserve chromosome integrity and influences PARP-inhibitor sensitivity in BRCA1/2-deficient cells.
- DDIAS binds phosphorylated TOPBP1 through its BRCT7/8 domains and is recruited to mitotic DNA-damage sites.
- DDIAS’s ssDNA-binding activity is required for CIP2A–TOPBP1 function and mitotic genome stability.
- ssDNA accumulated in BRCA1/2-deficient cells during G2—especially after PARP inhibition—is largely removed by prometaphase through a DDIAS- and DNA synthesis-dependent process.
- The findings establish the CIP2A–TOPBP1–DDIAS axis as a mitotic ssDNA-repair system distinct from canonical DNA-damage responses.