Plasmodesmata: a signaling hub at the cellular boundary

Lee, Jinkee

doi:10.1016/j.pbi.2015.06.019

Cited by 48 publications

(35 citation statements)

References 49 publications

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“…PD are viewed as signalling hub (Lee, 2015) and special membrane contact sites (MCSs) (Tilsner & Torrance, 2011;P erez-Sancho et al, 2016;Tilsner et al, 2016;Bayer et al, 2017;Brault et al, 2019), with lipid rafts or nanodomains (NDs) enriched in sterol and sphingolipids resident on the PD-PM (Raffaele et al, 2009;Mongrand et al, 2010;Tilsner & Torrance, 2011;Grison et al, 2015;Yan et al, 2019). Several functional proteins and signalling lipids are recruited to these NDs by lateral segregation to regulate PD permeability.…”

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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“…Mis-regulation of plasmodesmata function can lead to severe defects in organ growth and tissue patterning but also generate inappropriate responses to biotic and abiotic stresses [7,8,12,[15][16][17]. Plasmodesmata not only serve as conduits, but act as specialised signalling hubs, capable of generating and/or relaying signals from cell to cell through plasmodesmata-associated receptor activity [18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Multiple C2 domains and transmembrane region proteins ( MCTP s) tether membranes at plasmodesmata

et al. 2019

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In eukaryotes, membrane contact sites ( MCS ) allow direct communication between organelles. Plants have evolved a unique type of MCS , inside intercellular pores, the plasmodesmata, where endoplasmic reticulum ( ER )–plasma membrane ( PM ) contacts coincide with regulation of cell‐to‐cell signalling. The molecular mechanism and function of membrane tethering within plasmodesmata remain unknown. Here, we show that the multiple C2 domains and transmembrane region protein ( MCTP ) family, key regulators of cell‐to‐cell signalling in plants, act as ER ‐ PM tethers specifically at plasmodesmata. We report that MCTP s are plasmodesmata proteins that insert into the ER via their transmembrane region while their C2 domains dock to the PM through interaction with anionic phospholipids. A Atmctp3/Atmctp4 loss of function mutant induces plant developmental defects, impaired plasmodesmata function and composition, while MCTP 4 expression in a yeast Δtether mutant partially restores ER ‐ PM tethering. Our data suggest that MCTP s are unique membrane tethers controlling both ER ‐ PM contacts and cell‐to‐cell signalling.

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“…How plasmodesmata permeability is regulated during rice blast disease remains an open question. It is generally known that pathogen infections induce plasmodesmata closure by recruiting plasmodesmata-associated molecules such as callose (a β-1,3 glucan polymer) and that such plasmodesmata closure is linked to host immunity (Lee, 2015). In particular, recent studies in Arabidopsis thaliana suggest that recognition of chitin (pathogen-associated molecular pattern, PAMP, from fungal pathogens) by the chitin pattern recognition receptor LYM2 (also known as AtCEBiP) leads to plasmodesmata closure (Faulkner et al, 2013) and also that the plasmodesmata-localized protein 5 mediates callose deposition at plasmodesmata in a manner depending on the defense hormone salicylic acid (Lee and Lu, 2011).…”

Section: Discussionmentioning

confidence: 99%

Disruption of the interfacial membrane leads toMagnaporthe oryzaeeffector re-location and lifestyle switch during rice blast disease

Jones¹,

Zhu²,

Jenkinson³

et al. 2017

Preprint

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The hemibiotrophic fungus Magnaporthe oryzae produces invasive hyphae enclosed in a plant-derived interfacial membrane, known as the extra-invasive hyphal membrane (EIHM), in living rice cells. Little is known about when the EIHM is disrupted and how the disruption contributes to blast disease. Here we show that EIHM disruption correlates with the hyphal growth stage in first-invaded susceptible rice cells. Our approach utilized GFP secreted from invasive hyphae as an EIHM integrity reporter. Secreted-GFP accumulated in the EIHM compartment but appeared in the rice cytoplasm when the EIHM integrity was compromised. Live-cell imaging of secreted-GFP and various fluorescent reporters revealed that EIHM disruption led to rice vacuole rupture and cell death limited to the invaded cell with closed plasmodesmata. We report that EIHM disruption and host cell death are landmarks delineating three distinct infection phases (early biotrophic, late biotrophic, and transient necrotrophic phases) within the first-invaded cell before reestablishment of biotrophy in second-invaded cells. M. oryzae effectors exhibited phase-specific localizations, including entry of the apoplastic effector Bas4 into the rice cytoplasm during the late biotrophic phase. Understanding how the phase-specific dynamics are regulated and linked to host susceptibility will offer potential targets that can be exploited to control blast disease.

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Plasmodesmata: a signaling hub at the cellular boundary

Cited by 48 publications

References 49 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

Multiple C2 domains and transmembrane region proteins ( MCTP s) tether membranes at plasmodesmata

Disruption of the interfacial membrane leads toMagnaporthe oryzaeeffector re-location and lifestyle switch during rice blast disease

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