In the low-affinity actomyosin complex, nuclear myosin 1c interacts with SNF2h to activate RNA polymerase I transcription and cell cycle progression
(English)Article in journal (Refereed) Submitted
Actin and nuclear myosin 1C (NM1) cooperate as motor for RNA polymerase I transcription. NM1 is also part of the multiprotein assembly B-WICH required for transcription activation, containing the chromatin remodeling complex WICH with the subunits WSTF and SNF2h. Here we report that NM1 binds SNF2h, with enhanced affinity upon actin binding impairment. ChIP analysis revealed that NM1 and SNF2h gene occupancies require motor function and are transcription and cell cycle dependent. At onset of cell division when transcription is blocked B-WICH is disassembled due to WSTF phosphorylation to be reassembled at exit of mitosis on active gene in a WSTF-dependent manner. NM1 gene knockdown and motor function inhibition repressed rRNA synthesis by stalling polymerase and delayed cell cycle progression. Overall, these results point to a unique structural role for NM1 where in the low affinity actomyosin complex binding to SNF2h facilitates WICH assembly on rDNA for chromatin modifications and transcription activation.
nuclear myosin1, nuclear actin, SNF2h, WSTF, RNA polymerase I transcription
Research subject Cell Biology
IdentifiersURN: urn:nbn:se:su:diva-75270OAI: oai:DiVA.org:su-75270DiVA: diva2:515408