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Cana-Quijada, P.

Publications and source records attributed to Cana-Quijada, P..

4 recordsLinked to original sources

Extracellular vesicles associate with infectious geminiviral particles in the apoplast of infected plants.

Plant viruses have evolved diverse strategies to facilitate their movement and survival within the host. Among them, geminiviruses co-opt host cellular machinery to replicate and disseminate. Traditionally, viral propagation has been associated with intercellular symplastic trafficking mediated by plasmodesmata and viral movement proteins. However, recent evidence demonstrated that the plant RNA virus turnip mosaic virus (TuMV) components are associated with extracellular vesicles (EVs). EVs are membrane-bound structures secreted to the extracellular space to potentially mediate several plant-pathogen interactions such as cross-kingdom RNA interference or the delivery of stress response proteins. In animals, EVs facilitate viral transmission both within the host and across species, but knowledge about their potential roles in plant viral infection is scarce. In this study, we demonstrate that EVs isolated from geminivirus-infected plants contain complete viral genomes and both capsid and viral movement proteins. Furthermore, these EV fractions were demonstrated to be infectious when mechanically inoculated onto naive plants. This discovery suggests that EVs may serve as alternative carriers for geminivirus components, enabling long-range transport or potentially modulating host immune responses, and highlights geminiviral capacity to transverse membrane boundaries, essential for circulative arbovirus propagation in their insect vectors. Significance StatementViruses are obligate intracellular parasites that shape ecological communities and crucially challenge animal and plant health worldwide. Conversely to animal viruses, plant-infecting viruses rely on plasmodesmata to disseminate through their host and establish systemic infection. Nonetheless, most plant viruses are insect-transmitted whose ecological cycle relies on their insect vector spread. Thus, strategies to cross continuous membrane barriers are essential for their dissemination and may be potentially conserved in plant hosts. Our discovery that infectious viral entities are associated with EVs reveals an alternative pathway for geminiviral movement within plant hosts that could facilitate vector transmission, challenging our long-standing understanding of plant virus biology and expanding the current conception of plant viral pathology.

plant biology↗

Defender or accomplice? Dual roles of plant vesicle trafficking in restricting and enabling geminiviral systemic infection.

The vesicle trafficking system enables multidirectional cargo fluxes between endomembrane compartments, ensuring the viability of eukaryotic cells. However, vesicle trafficking plays dual roles during pathogen infections. In plants, the endomembrane system mediates autophagic immune responses but can also be hijacked by pathogens to facilitate successful infections. In this study, we demonstrate that vesicle trafficking machinery acts as a double-edged sword during infection by the geminivirus tomato yellow leaf curl Sardinia virus (TYLCSaV) in Nicotiana benthamiana. Virus-induced gene silencing (VIGS) of eight genes encoding key vesicle trafficking regulators revealed contrasting outcomes. Silencing of NbSAR1 and NbAP-1{gamma} significantly increased systemic geminiviral DNA accumulation, whereas silencing of Nb{delta}-COP, NbARF1, and clathrin genes almost completely abolished infection. Notably, this inhibition is hypothesized to result from direct or indirect impairment in viral movement, as replication remained unaffected by gene silencing. Furthermore, the observed effects affect other geminiviruses, including tomato yellow leaf curl virus (TYLCV) and beet curly top virus (BCTV), but not unrelated pathogens such as the RNA potato virus X (PVX) or the plant pathogenic bacterium Pseudomonas syringae. These findings suggest that while the vacuolar and autophagy branches of the vesicle trafficking system might mediate antiviral autophagic defense responses, the integrity of endocytosis and retrograde transport is essential for systemic geminiviral infection.

plant biology↗

Plasmodesmata act as unconventional membrane contact sites regulating inter-cellular molecular exchange in plants

Membrane contact sites (MCS) are fundamental for intracellular communication, but their role in intercellular communication remains unexplored. We show that in plants, plasmodesmata communication bridges function as atypical endoplasmic reticulum (ER)-plasma membrane (PM) tubular MCS, operating at cell-cell interfaces. Similar to other MCS, ER-PM apposition is controlled by a protein-lipid tethering complex, but uniquely, this serves intercellular communication. Combining high-resolution microscopy, molecular dynamics, pharmacological and genetic approaches, we show that cell-cell trafficking is modulated through the combined action of Multiple C2 domains and transmembrane domain proteins (MCTP) 3, 4, and 6 ER-PM tethers, and phosphatidylinositol-4-phosphate (PI4P) lipid. Graded PI4P amounts regulate MCTP docking to the PM, their plasmodesmata localization and cell-cell permeability. SAC7, an ER-localized PI4P-phosphatase, regulates MCTP4 accumulation at plasmodesmata and modulates cell-cell trafficking capacity in a cell-type specific manner. Our findings expand MCSs functions in information transmission, from intracellular to intercellular cellular activities. In briefPlant intercellular communication is regulated via tubular membrane contact through PI4P binding-ER-PM tether MCTP proteins HighlightsO_LIPlasmodesmata are unconventional ER/PM tubular contact sites located at cell-cell interface C_LIO_LIPlasmodesmata operate as control valves, modulating ER-PM contacts to regulate transport C_LIO_LIMCTP3, MCTP4, MCTP6 and PI4P tethering elements act as valve regulators C_LIO_LISAC7 PI4P phosphatase controls plasmodesmata MCS in a cell-type-specific manner C_LI

plant biology↗

The transcriptional regulator JAZ8 interacts with the C2 protein from geminiviruses and limits the viral infection in Arabidopsis

Jasmonates (JAs) are phytohormones that finely regulate critical biological processes, including plant development and defense. JASMONATE ZIM-DOMAIN (JAZ) proteins are crucial keeping JA-responsive genes in a repressed state. In the presence of JA-Ile, JAZ repressors are ubiquitinated and targeted for degradation by the ubiquitin/proteasome system, allowing the activation of the downstream transcription factors and, consequently, the activation of JA-responsive genes. A growing body of evidence has shown that JA signalling is crucial in defending against plant viruses and their insect vectors. Here, we describe the interaction of C2 proteins from two geminiviruses from the genus Begomovirus, tomato yellow curl Sardinia virus (TYLCSaV) and tomato yellow leaf curl virus (TYLCV), with the transcriptional repressor JAZ8 from Arabidopsis thaliana and its closest orthologue in tomato, SlJAZ9. Both JAZ and C2 proteins colocalize in the nucleus, forming discrete nuclear speckles. Overexpression of JAZ8 did not lead to altered responses to TYLCV infection; however, knock-down of JAZ8 favours the geminiviral infection in plants. Low levels of JAZ8 likely affect the viral infection specifically since JAZ8-silenced plants do not display developmental phenotypes nor present differences in their interaction with the viral insect vector. Our results show that JAZ8 interacts with geminiviral C2 proteins and exerts an anti-geminiviral effect.

plant biology↗