tetano
Editor, Senior Moderator
Nat Commun
. 2024 Dec 30;15(1):10805.
doi: 10.1038/s41467-024-55034-y. Human ANP32A/B are SUMOylated and utilized by avian influenza virus NS2 protein to overcome species-specific restriction
Liuke Sun[SUP] 1 [/SUP], Xing Guo[SUP] 1 [/SUP], Mengmeng Yu[SUP] 1 [/SUP], Xue-Feng Wang[SUP] 1 [/SUP], Huiling Ren[SUP] 1 [/SUP], Xiaojun Wang[SUP] 2 3 [/SUP]
Affiliations
Human ANP32A/B (huANP32A/B) poorly support the polymerase activity of avian influenza viruses (AIVs), thereby limiting interspecies transmission of AIVs from birds to humans. The SUMO-interacting motif (SIM) within NS2 promotes the adaptation of AIV polymerase to huANP32A/B via a yet undisclosed mechanism. Here we show that huANP32A/B are SUMOylated by the E3 SUMO ligase PIAS2α, and deSUMOylated by SENP1. SUMO modification of huANP32A/B results in the recruitment of NS2, thereby facilitating huANP32A/B-supported AIV polymerase activity. Such a SUMO-dependent recruitment of NS2 is mediated by its association with huANP32A/B via the SIM-SUMO interaction module, where K68/K153-SUMO in huANP32A or K68/K116-SUMO in huANP32B interacts with the NS2-SIM. The SIM-SUMO-mediated interactions between NS2 and huANP32A/B function to promote AIV polymerase activity by positively regulating AIV vRNP-huANP32A/B interactions and AIV vRNP assembly. Our study offers insights into the mechanism of NS2-SIM in facilitating AIVs adaptation to mammals.
. 2024 Dec 30;15(1):10805.
doi: 10.1038/s41467-024-55034-y. Human ANP32A/B are SUMOylated and utilized by avian influenza virus NS2 protein to overcome species-specific restriction
Liuke Sun[SUP] 1 [/SUP], Xing Guo[SUP] 1 [/SUP], Mengmeng Yu[SUP] 1 [/SUP], Xue-Feng Wang[SUP] 1 [/SUP], Huiling Ren[SUP] 1 [/SUP], Xiaojun Wang[SUP] 2 3 [/SUP]
Affiliations
- PMID: 39737943
- PMCID: PMC11686252
- DOI: 10.1038/s41467-024-55034-y
Human ANP32A/B (huANP32A/B) poorly support the polymerase activity of avian influenza viruses (AIVs), thereby limiting interspecies transmission of AIVs from birds to humans. The SUMO-interacting motif (SIM) within NS2 promotes the adaptation of AIV polymerase to huANP32A/B via a yet undisclosed mechanism. Here we show that huANP32A/B are SUMOylated by the E3 SUMO ligase PIAS2α, and deSUMOylated by SENP1. SUMO modification of huANP32A/B results in the recruitment of NS2, thereby facilitating huANP32A/B-supported AIV polymerase activity. Such a SUMO-dependent recruitment of NS2 is mediated by its association with huANP32A/B via the SIM-SUMO interaction module, where K68/K153-SUMO in huANP32A or K68/K116-SUMO in huANP32B interacts with the NS2-SIM. The SIM-SUMO-mediated interactions between NS2 and huANP32A/B function to promote AIV polymerase activity by positively regulating AIV vRNP-huANP32A/B interactions and AIV vRNP assembly. Our study offers insights into the mechanism of NS2-SIM in facilitating AIVs adaptation to mammals.