Abstract

The matrix protein M1 of the Influenza A virus (IAV) is supposed to mediate viral assembly and budding at the plasma membrane (PM) of infected cells. In order for a new viral particle to form, the PM lipid bilayer has to bend into a vesicle toward the extracellular side. Studies in cellular models have proposed that different viral proteins might be responsible for inducing membrane curvature in this context (including M1), but a clear consensus has not been reached. In the present study, we use a combination of fluorescence microscopy, cryogenic transmission electron microscopy (cryo-TEM), cryo-electron tomography (cryo-ET) and scanning fluorescence correlation spectroscopy (sFCS) to investigate M1-induced membrane deformation in biophysical models of the PM. Our results indicate that M1 is indeed able to cause membrane curvature in lipid bilayers containing negatively charged lipids, in the absence of other viral components. Furthermore, we prove that protein binding is not sufficient to induce membrane restructuring. Rather, it appears that stable M1–M1 interactions and multimer formation are required in order to alter the bilayer three-dimensional structure, through the formation of a protein scaffold. Finally, our results suggest that, in a physiological context, M1-induced membrane deformation might be modulated by the initial bilayer curvature and the lateral organization of membrane components (i.e. the presence of lipid domains).

Highlights

  • The Influenza A virus (IAV) buds from the plasma membrane (PM) of infected cells and, while doing so, acquires a lipid envelope from its host [1,2,3,4]

  • In order to clarify whether M1 is sufficient to induce membrane deformation in protein-free lipid bilayers, we incubated giant unilamellar vesicle (GUV) of different compositions in the presence of 5 μM M1-Alexa448

  • In order to release a new virion from the PM of an infected cell, the lipid bilayer has to undergo a shape change

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Summary

Introduction

The Influenza A virus (IAV) buds from the plasma membrane (PM) of infected cells and, while doing so, acquires a lipid envelope from its host [1,2,3,4]. The process by which M1 or other viral proteins can induce membrane curvature during IAV budding is less clear This issue has been investigated in cellulo without reaching a clear consensus [11]. Other studies have shown instead that IAV hemagglutinin and neuraminidase are needed to produce viral particles, while M1 might not play a significant role [14,15,16]. Another group suggested that, in the presence of significant M1–PM binding, the protein

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