StREM1.3 REMORIN Protein Plays an Agonistic Role in Potyvirus Cell-to-Cell Movement in N. benthamiana.

Marion Rocher,Anne-Flore Deroubaix,Luc Sofer,Vincent Simon,Véronique Germain,Marie-Dominique Jolivet,Sébastien Mongrand,Sylvie German-Retana

doi:10.3390/v14030574

Abstract

REMORIN proteins belong to a plant-specific multigene family that localise in plasma membrane nanodomains and in plasmodesmata. We previously showed that in Nicotiana benthamiana, group 1 StREM1.3 limits the cell-to-cell spread of a potexvirus without affecting viral replication. This prompted us to check whether an effect on viral propagation could apply to potyvirus species Turnip mosaic virus (TuMV) and Potato virus A (PVA). Our results show that StREM1.3 transient or stable overexpression in transgenic lines increases potyvirus propagation, while it is slowed down in transgenic lines underexpressing endogenous NbREMs, without affecting viral replication. TuMV and PVA infection do not alter the membranous localisation of StREM1.3. Furthermore, StREM1.3-membrane anchoring is necessary for its agonist effect on potyvirus propagation. StREM1.3 phosphocode seems to lead to distinct plant responses against potexvirus and potyvirus. We also showed that StREM1.3 interacts in yeast and in planta with the key potyviral movement protein CI (cylindrical inclusion) at the level of the plasma membrane but only partially at plasmodesmata pit fields. TuMV infection also counteracts StREM1.3-induced plasmodesmata callose accumulation at plasmodesmata. Altogether, these results showed that StREM1.3 plays an agonistic role in potyvirus cell-to-cell movement in N. benthamiana.

Highlights

To invade the whole plant after replication, plant viruses must move intracellularly to reach the plasmodesmata (PD), the symplasmic channels between plant cells that are the gateway for this movement
We previously showed that in tomato and N. benthamiana, StREM1.3 limits the cell-tocell spread of the potexvirus PVX without affecting its replication [40]
35S::GFP–REM1.3 overexpressing transgenic lines leads to an increase in the surface of infection foci induced by Turnip mosaic virus (TuMV) in the inoculated leaves

Summary

Introduction

To invade the whole plant after replication, plant viruses must move intracellularly to reach the plasmodesmata (PD), the symplasmic channels between plant cells that are the gateway for this movement. One mechanism, exemplified by the 30K-type MP of Tobacco mosaic virus (TMV), may be common to all viruses that do not move as intact virions, including the triple gene block proteins (TGBps) of potexviruses and hordeiviruses. Those viruses are considered as “non-tubule-forming viruses”, which do not morphologically drastically alter PD. The MPs of these viruses form large tubules that insert into PD to allow the transport of intact viruses between cells Those viruses are considered “tubule-forming viruses”, which induce drastic alteration in PD, with the elimination of the desmotubule

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Conclusion