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KCTD10 resolves co-directional transcription–replication conflicts
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DOI：10.1016/j.tcb.2026.04.010.png)
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Abstract
En 中文
Co-directional transcription–replication conflicts are frequent but relatively understudied sources of genomic stress. KCTD10 functions as a bivalent sensor that links replication and transcription machineries at sites of conflict. The Cullin 3–Potassium channel tetramerization domain containing 10 (KCTD10) complex remodels RNA polymerase II through nonproteolytic ubiquitination to enable replisome progression. Conflict sensing is coupled to Ataxia telangiectasia mutated (ATM)–Checkpoint kinase 2 (CHK2) signaling, integrating local resolution with global replication stress responses. Co-directional conflicts act as regulated genomic hubs, balancing replication speed with transcriptional fidelity and revealing potential therapeutic vulnerabilities.
Keywords:
KCTD10
transcription–replication conflicts
replication stress
RNA polymerase II
ATM-CHK2 signaling
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