The 7SK small nuclear ribonucleoprotein links the cell responses to transcription and replication stress by promoting replication fork reversal and homologous recombination.

7SK-snRNP promotes replication fork slowing and RAD51-mediated replication fork reversal under replication-plus-transcription stress, supporting homologous recombination at replication-associated breaks.

• Why it matters: Transcription-blocking conditions often trigger replication stress and DSBs, but how 7SK-snRNP components coordinate RNAPII activity with RAD51 functions during these conflicts is unclear.
• What they did: The study tested 7SK-snRNP component roles in replication stress responses, measuring replication fork behavior, RAD51 recruitment to replication-associated DSBs or gaps, and homologous recombination at direct DSBs, including hydroxyurea controls.
• The result: 7SK-snRNP components are not required for RAD51 recruitment in response to hydroxyurea, are not recruited to stressed replication forks, and RNAPII inhibition phenocopies their loss, linking RNAPII modulation to multiple RAD51 functions under transcription stress.

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