Summary: In photosynthetic cells, plants convert carbon dioxide to sugars that can be moved between cellular compartments by transporters before being subsequently metabolized to support plant growth and development. Most pathogens cannot synthesize sugars directly but have evolved mechanisms to obtain plant‐derived sugars as C resource for successful infection and colonization. The availability of sugars to pathogens can determine resistance or susceptibility. Here, we summarize current progress on the roles of sugar transporters in plant–pathogen interactions. We highlight how transporters are manipulated antagonistically by both host and pathogens in competing for sugars. We examine the potential application of this target in resistance breeding and discuss opportunities and challenges for the future.

Plants are constantly exposed to diverse microbes and thus develop a sophisticated perceive system to distinguish non-self from self and identify non-self as friends or foes. Plants can detect microbes in apoplast via recognition of microbe-associated molecular patterns (MAMPs) by pattern recognition receptors (PRRs) on the cell surface to activate appropriate signaling in response to microbes. MAMPs are highly conserved but essential molecules of microbes and often buried in microbes’ complex structure. Mature MAMPs are released from microbes by invasion-induced hydrolytic enzymes in apoplast and accumulate in proximity of plasma membrane-localized PRRs to be perceived as ligands to activate downstream signaling. In response, microbes developed strategies to counteract these processing. Here, we review how the form, the concentration, and the size of mature MAMPs affect the PRR-mediated immune signaling. In particular, we describe some potential applications and explore potential open questions in the fields.

Summary: Wood is the most important repository of assimilated carbon in the biosphere, in the form of large polymers (cellulose, hemicelluloses including glucuronoxylan, and lignin) that interactively form a composite, together with soluble extractives including phenolic and aliphatic compounds. Molecular interactions among these compounds are not fully understood. We have targeted the expression of a fungal α‐glucuronidase to the wood cell wall of aspen (Populus tremulaL. × tremuloidesMichx.) and Arabidopsis (Arabidopsis thaliana(L.) Heynh), to decrease contents of the 4‐O‐methyl glucuronopyranose acid (mGlcA) substituent of xylan, to elucidate mGlcA's functions. The enzyme affected the content of aliphatic insoluble cell wall components having composition similar to suberin, which required mGlcA for binding to cell walls. Such suberin‐like compounds have been previously identified in decayed wood, but here, we show their presence in healthy wood of both hardwood and softwood species. By contrast, γ‐ester bonds between mGlcA and lignin were insensitive to cell wall‐localized α‐glucuronidase, supporting the intracellular formation of these bonds. These findings challenge the current view of the wood cell wall composition and reveal a novel function of mGlcA substituent of xylan in fastening of suberin‐like compounds to cell wall. They also suggest an intracellular initiation of lignin–carbohydrate complex assembly.

In plants, plasmodesmata establish cytoplasmic continuity between cells to allow for communication and resource exchange across the cell wall. While plant pathogens use plasmodesmata as a pathway for both molecular and physical invasion, the benefits of molecular invasion (cell-to-cell movement of pathogen effectors) are poorly understood. To establish a methodology for identification and characterization of the cell-to-cell mobility of effectors, we performed a quantitative live imaging-based screen of candidate effectors of the fungal pathogen Colletotrichum higginsianum. We predicted C. higginsianum effectors by their expression profiles, the presence of a secretion signal, and their predicted and in planta localization when fused to green fluorescent protein. We assayed for cell-to-cell mobility of nucleocytosolic effectors and identified 14 that are cell-to-cell mobile. We identified that three of these effectors are “hypermobile,” showing cell-to-cell mobility greater than expected for a protein of that size. To explore the mechanism of hypermobility, we chose two hypermobile effectors and measured their impact on plasmodesmata function and found that even though they show no direct association with plasmodesmata, each increases the transport capacity of plasmodesmata. Thus, our methods for quantitative analysis of cell-to-cell mobility of candidate microbe-derived effectors, or any suite of host proteins, can identify cell-to-cell hypermobility and offer greater understanding of how proteins affect plasmodesmal function and intercellular connectivity. [ ] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY 4.0 International license .

Plasmodesmata (PD) are dynamic nanochannels interconnecting plant cells and coordinating development, nutrient distribution, and systemic defense. Their permeability is tightly regulated by callose turnover, PD-localized proteins, lipid microdomains, and endoplasmic reticulum (ER)–plasma membrane (PM) tethers, which together form regulatory nodes that gate symplastic exchange. Increasing evidence demonstrates that effectors from diverse kingdoms—fungi, oomycetes, bacteria, viruses, viroids, phytoplasmas, nematodes, insects, parasitic plants, and symbiotic microbes—converge on these same nodes to modulate PD gating. Pathogens typically suppress callose deposition or destabilize PD regulators to keep channels open, whereas mutualists fine-tune PD conductivity to balance resource exchange with host immunity. This review synthesizes current knowledge of effector strategies that remodel PD architecture or exploit PD for intercellular movement, highlighting novel cross-kingdom commonalities–callose manipulation, reprogramming of PD proteins, lipid rewiring, and co-option of ER-PM tethers. We outline unresolved questions on effector–PD target specificity and dynamics, and identify prospects in imaging, proteomics, and synthetic control of PD. Understanding how effectors reprogram PD connectivity can enable engineering of crops that block pathogenic trafficking while safeguarding beneficial symbioses.