EMD-17783

Single-particle
2.88 Å
EMD-17783 Deposition: 30/06/2023
Map released: 21/02/2024
Last modified: 13/11/2024
Overview 3D View Sample Experiment Validation Volume Browser Additional data Links
Overview 3D View Sample Experiment Validation Volume Browser Additional data Links

EMD-17783

Influenza A/H7N9 polymerase in elongation state with continuous Pol II pS5 CTD peptide mimic bound in site 1A/2A

EMD-17783

Single-particle
2.88 Å
EMD-17783 Deposition: 30/06/2023
Map released: 21/02/2024
Last modified: 13/11/2024
Overview 3D View Sample Experiment Validation Volume Browser Additional data Links
Sample Organism: Influenza A virus (A/Zhejiang/DTID-ZJU01/2013(H7N9)), Homo sapiens
Sample: Influenza A/H7N9 polymerase in replicase-like conformation in pre-initiation state with Pol II pS5 CTD peptide mimic bound in site 1A/2A
Fitted models: 8pnq (Avg. Q-score: 0.586)

Deposition Authors: Arragain B , Cusack S
The host RNA polymerase II C-terminal domain is the anchor for replication of the influenza virus genome.
Krischuns T , Arragain B , Isel C , Paisant S, Budt M , Wolff T , Cusack S , Naffakh N
(2024) Nat Commun , 15 , 1064 - 1064
PUBMED: 38316757
DOI: doi:10.1038/s41467-024-45205-2
ISSN: 2041-1723
Abstract:
The current model is that the influenza virus polymerase (FluPol) binds either to host RNA polymerase II (RNAP II) or to the acidic nuclear phosphoprotein 32 (ANP32), which drives its conformation and activity towards transcription or replication of the viral genome, respectively. Here, we provide evidence that the FluPol-RNAP II binding interface, beyond its well-acknowledged function in cap-snatching during transcription initiation, has also a pivotal role in replication of the viral genome. Using a combination of cell-based and in vitro approaches, we show that the RNAP II C-terminal-domain, jointly with ANP32, enhances FluPol replication activity. We observe successive conformational changes to switch from a transcriptase to a replicase conformation in the presence of the bound RNPAII C-terminal domain and propose a model in which the host RNAP II is the anchor for transcription and replication of the viral genome. Our data open new perspectives on the spatial coupling of viral transcription and replication and the coordinated balance between these two activities.