Turnip Mosaic Virus Uses the SNARE Protein VTI11 in an Unconventional Route for Replication Vesicle Trafficking

Cabanillas, Daniel Garcia; Jiang, Jianan; Movahed, Nooshin; Germain, Hugo; Yamaji, Yutaka; Zheng, Huanquan; Laliberté, Jean‐François

doi:10.1105/tpc.18.00281

Cited by 57 publications

(87 citation statements)

References 93 publications

(151 reference statements)

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“…In addition to REMs which may control the ND components involved in signal recognition and transduction (Jarsch & Ott, 2011;Gui et al, 2016;Ott, 2017), callose synthase (CalS) via transmembrane domains, callose-binding proteins (PDCBs) or b-1,3-glucanases (PDBGs) via a glycophosphatidylinositol anchor target PD-PM to regulate callose deposition (Simpson et al, 2009;Benitez-Alfonso et al, 2013). Synaptotagmin A (SYTA), component of MCS, is recruited to PD upon viral infection and involved in the formation of MCS and cell-to-cell movement of viruses including TuMV (Lewis & Lazarowitz, 2010;Uchiyama et al, 2014;Amarjeet et al, 2015;Amit et al, 2015;Li et al, 2017;Cabanillas et al, 2018). As for lipids, PtdInsPs are present in PD (Grison et al, 2015) and capable of sequestering PCaP1 from actin filaments (Nagasaki et al, 2008;Qin et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Remorin interacting with PCaP1 impairs Turnip mosaic virus intercellular movement but is antagonised by VPg

et al. 2019

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Group 1 Remorins (REMs) are extensively involved in virus trafficking through plasmodesmata (PD). However, their roles in Potyvirus cell-to-cell movement are not known. The plasma membrane (PM)-associated Ca 2+ binding protein 1 (PCaP1) interacts with the P3N-PIPO of Turnip mosaic virus (TuMV) and is required for TuMV cell-to-cell movement, but the underlying mechanism remains elusive.The mutant plants with overexpression or knockout of REM1.2 were used to investigate its role in TuMV cell-to-cell movement. Arabidopsis thaliana complementary mutants of pcap1 were used to investigate the role of PCaP1 in TuMV cell-to-cell movement. Yeast-two-hybrid, bimolecular fluorescence complementation, co-immunoprecipitation and RT-qPCR assays were employed to investigate the underlying molecular mechanism.The results show that TuMV-P3N-PIPO recruits PCaP1 to PD and the actin filament-severing activity of PCaP1 is required for TuMV intercellular movement. REM1.2 negatively regulates the cell-to-cell movement of TuMV via competition with PCaP1 for binding actin filaments. As a counteractive response, TuMV mediates REM1.2 degradation via both 26S ubiquitin-proteasome and autophagy pathways through the interaction of VPg with REM1.2 to establish systemic infection in Arabidopsis.This work unveils the actin cytoskeleton and PM nanodomain-associated molecular events underlying the cell-to-cell movement of potyviruses.

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Section: Discussionmentioning

confidence: 99%

Remorin interacting with PCaP1 impairs Turnip mosaic virus intercellular movement but is antagonised by VPg

et al. 2019

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“…Typically, plant virus replication on membranes induces strong membrane modifications and is associated with interference of virus infection with lipid metabolism and membrane targeting and transport (Altan‐Bonnet, ; De Castro et al , ; Nagy, ; Nagy and Pogany, ; Zhang et al ., , ). Infection by diverse plant viruses has been shown to imply membrane fusion processes (Garcia Cabanillas et al ., ; Huang et al ., ; Wei et al ., ) as well as conventional and unconventional protein transport routes (Diaz et al ., ; Grangeon et al ., ; Kovalev et al ., ; Movahed et al ., ; Ribeiro et al ., ; Wang et al ., ; Wei and Wang, ).…”

Section: Introductionmentioning

confidence: 99%

Perception of double‐stranded RNA in plant antiviral immunity

Niehl

Heinlein

2019

Molecular Plant Pathology

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Summary RNA silencing and antiviral pattern‐triggered immunity (PTI) both rely on recognition of double‐stranded (ds)RNAs as defence‐inducing signals. While dsRNA recognition by dicer‐like proteins during antiviral RNA silencing is thoroughly investigated, the molecular mechanisms involved in dsRNA perception leading to antiviral PTI are just about to be untangled. Parallels to antimicrobial PTI thereby only partially facilitate our view on antiviral PTI. PTI against microbial pathogens involves plasma membrane bound receptors; however, dsRNAs produced during virus infection occur intracellularly. Hence, how dsRNA may be perceived during this immune response is still an open question. In this short review, we describe recent discoveries in PTI signalling upon sensing of microbial patterns and endogenous ‘danger’ molecules with emphasis on immune signalling‐associated subcellular trafficking processes in plants. Based on these studies, we develop different scenarios how dsRNAs could be sensed during antiviral PTI.

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“…These viral replication vesicles are generated in the ER and are released at the ER exit sites (Wei and Wang, 2008;Jiang et al, 2015). They are believed to take a Golgi bypass unconventional pathway (Cabanillas et al, 2018) that requires microfilaments to reach plasmodesmata (PD; Cotton et al, 2009) where they ultimately move into uninfected neighboring cells . These viral vesicles generated early in the infection process are usually convolutional membrane structures (CM) still linked to the ER (Wan et al, 2015a).…”

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confidence: 99%

A Host ER Fusogen Is Recruited by Turnip Mosaic Virus for Maturation of Viral Replication Vesicles

et al. 2018

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Like other positive-strand RNA viruses, the Turnip mosaic virus (TuMV) infection leads to the formation of viral vesicles at the endoplasmic reticulum (ER). Once released from the ER, the viral vesicles mature intracellularly and then move intercellularly. While it is known that the membrane-associated viral protein 6K2 plays a role in the process, the contribution of host proteins has been poorly defined. In this article, we show that 6K2 interacts with RHD3, an ER fusogen required for efficient ER fusion. When RHD3 is mutated, a delay in the development of TuMV infection is observed. We found that the replication of TuMV and the cell-to-cell movement of its replication vesicles are impaired in rhd3. This defect can be tracked to a delayed maturation of the viral vesicles from the replication incompetent to the competent state. Furthermore, 6K2 can relocate RHD3 from the ER to viral vesicles. However, a Golgi-localized mutated 6K2 GV is unable to interact and relocate RHD3 to viral vesicles. We conclude that the maturation of TuMV replication vesicles requires RHD3 for efficient viral replication and movement.

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Turnip Mosaic Virus Uses the SNARE Protein VTI11 in an Unconventional Route for Replication Vesicle Trafficking

Cited by 57 publications

References 93 publications

Remorin interacting with PCaP1 impairs Turnip mosaic virus intercellular movement but is antagonised by VPg

Remorin interacting with PCaP1 impairs Turnip mosaic virus intercellular movement but is antagonised by VPg

Perception of double‐stranded RNA in plant antiviral immunity

A Host ER Fusogen Is Recruited by Turnip Mosaic Virus for Maturation of Viral Replication Vesicles

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