Plasmodesmata-Involved Battle Against Pathogens and Potential Strategies for Strengthening Hosts

Abstract

Plasmodesmata (PD) are membrane-lined pores that connect adjacent cells to mediate symplastic communication in plants. These intercellular channels enable cell-to-cell trafficking of various molecules essential for plant development and stress responses, but they can also be utilized by pathogens to facilitate their infection of hosts. Some pathogens or their effectors are able to spread through the PD by modifying their permeability. Yet plants have developed various corresponding defense mechanisms, including the regulation of PD to impede the spread of invading pathogens. In this review, we aim to illuminate the various roles of PD in the interactions between pathogens and plants during the infection process. We summarize the pathogenic infections involving PD and how the PD could be modified by pathogens or hosts. Furthermore, we propose several hypothesized and promising strategies for enhancing the disease resistance of host plants by the appropriate modulation of callose deposition and plasmodesmal permeability based on current knowledge.

Action Mechanisms of Effectors in Plant-Pathogen Interaction

“…Under immune stimulation, plants shut down PD as part of their immune response, which is also used by pathogens to facilitate their infection of the host. The effector transfer pathway via PD is critical for the successful plant colonization by pathogens [ 81 , 82 , 83 ].…”

Pathogen effectors: What do they do at plasmodesmata?

“…Given that the translocation of effectors through PD is necessary for the success of plant colonization by several pathogens (Cao et al, 2018 ; Liu et al, 2021 ), effectors have employed multiple strategies to attack PD‐callose regulation. To counter PD closure and callose accumulation, effectors can target the PD (Cao et al, 2018 ; Rahman et al, 2021 ; Tomczynska et al, 2020 ), thereby enlarging the PD gate.…”

“…In parallel to the cell‐autonomous immune system, the non‐cell‐autonomous immune system responds to the pathogens via signals delivered from infected cells to uninfected cells through apoplastic and symplasmic routes (Lee & Lu, 2011 ; Yan et al, 2019 ). It has been proposed that deposition of callose at PD determines the effectiveness of some pathogen effectors and the movement of signalling molecules from one cell to neighbouring cells (Cheval & Faulkner, 2018 ; Li et al, 2021 ; Liu et al, 2021 ). Interestingly, a recent study showed that several effectors from Pseudomonas syringae move from one cell to another cell through PD (Li et al, 2021 ).…”

The primary function of Six5 of Fusarium oxysporum is to facilitate Avr2 activity by together manipulating the size exclusion limit of plasmodesmata

“…The number of PD in root tissue, often an entry point for plant pathogens, increases from the epidermis toward the vascular tissues (Burch-Smith et al, 2011). Manipulation of PD channels can among others, benefit the spread of viral particles, fungal hyphae, or translocation of effector proteins to neighboring cells to potentially suppress immune responses (Benitez-Alfonso et al, 2010;Cheval and Faulkner, 2018;Liu et al, 2021). Although PD manipulation by viruses has been studied extensively, how filamentous pathogens manipulate PD with the aid of intracellular effectors is a relatively new and unexplored field (Liu et al, 2021).…”

“…Manipulation of PD channels can among others, benefit the spread of viral particles, fungal hyphae, or translocation of effector proteins to neighboring cells to potentially suppress immune responses (Benitez-Alfonso et al, 2010;Cheval and Faulkner, 2018;Liu et al, 2021). Although PD manipulation by viruses has been studied extensively, how filamentous pathogens manipulate PD with the aid of intracellular effectors is a relatively new and unexplored field (Liu et al, 2021). Effector proteins PWL2 and BAS1 of the rice blast fungus Magnaporthe oryzae spread into uninfected cells through PD when delivered into the cytoplasm of rice cells via a biotrophic interfacial complex (BIC) (Khang et al, 2010).…”