TY - JOUR TI - Influenza virus recruits host protein kinase C to control assembly and activity of its replication machinery AU - Mondal, Arindam AU - Dawson, Anthony R AU - Potts, Gregory K AU - Freiberger, Elyse C AU - Baker, Steven F AU - Moser, Lindsey A AU - Bernard, Kristen A AU - Coon, Joshua J AU - Mehle, Andrew A2 - Kirkegaard, Karla VL - 6 PY - 2017 DA - 2017/07/31 SP - e26910 C1 - eLife 2017;6:e26910 DO - 10.7554/eLife.26910 UR - https://doi.org/10.7554/eLife.26910 AB - Influenza virus expresses transcripts early in infection and transitions towards genome replication at later time points. This process requires de novo assembly of the viral replication machinery, large ribonucleoprotein complexes (RNPs) composed of the viral polymerase, genomic RNA and oligomeric nucleoprotein (NP). Despite the central role of RNPs during infection, the factors dictating where and when they assemble are poorly understood. Here we demonstrate that human protein kinase C (PKC) family members regulate RNP assembly. Activated PKCĪ“ interacts with the polymerase subunit PB2 and phospho-regulates NP oligomerization and RNP assembly during infection. Consistent with its role in regulating RNP assembly, knockout of PKCĪ“ impairs virus infection by selectively disrupting genome replication. However, primary transcription from pre-formed RNPs deposited by infecting particles is unaffected. Thus, influenza virus exploits host PKCs to regulate RNP assembly, a step required for the transition from primary transcription to genome replication during the infectious cycle. KW - influenza virus KW - nucleoprotein KW - polymerase KW - kinase KW - protein kinase C JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -