Plants are autotrophs that synthesize sugars through photocontractualization. Plant pathogens are heterotrophs that must obtain a sugar source from the host plant in order to successfully establish an infestation. Due to the limited carbon source in the host plant, the pathogen must compete with the plant for the sugar source to maintain its infection. Conversely, plants often limit the supply of sugar sources to the pathogen and inhibit infection. Therefore, how plants and pathogens compete for limited sugar sources by antagonistically manipulating the supply of sugar sources becomes the key to susceptibility or resistance. On June 16, 2024, Liu Xiaokun's team from Lushan Botanical Garden and Professor Tony Miller's team from John Innas Center published a review paper entitled "The role of sugar transporters in the battle for carbon between plants and pathogens" in the internationally renowned Journal of Plant Biotechnology. This paper expounds the research progress on the role of glycotransporters in plant-pathogen interactions, and summarizes how pathogens and plants antagonistically manipulate transporters to compete for carbohydrate nutrition.
When pathogenic bacteria infect plants, there are two transport routes for sugars from the surrounding tissues to the infection site: the apoplast pathway and the symplast pathway. In the apoplast pathway of carbohydrate transport, distal carbohydrates are transported by transporters to apoplast and then spread to the point of infection. In the symplast carbohydrate transport pathway, distal carbohydrates move to the point of infection via a symplast consisting of plasmodesmata and cell membrane. Subsequently, according to the type of pathogenic bacteria, the type of life history and the period of infection, they are absorbed by the pathogenic bacteria in different ways.
Figure 1. When plants interact with pathogenic bacteria, there are two pathways for the movement of sugars in plants
There are three main types of glycotransporters in plants: SWEETs, SUTs, and STPs. They are localized to specific subcellular membranes and have specific sugar substrates and transport functions. In response to internal growth and development signals and external stimuli, plants use these glycotransporters to regulate the transport, distribution and supply of sugars in conjunction with different invertases. For example, sucrose can be transported by SWEET to the apoplast and then transported back into the cell by the SUT. Extracellular sucrose can be broken down into monosaccharides by cell wall sugar invertase. These monosaccharides are transported back into the cell by STP. Intracellular sucrose can be degraded into monosaccharides by neutral glycosinvertase. Vacuolar membranes are also involved in the transport and distribution of sugars. For example, intracellular sucrose can be degraded into monosaccharides by vesolar invertase, which is then excreted into the extravacuolar cytoplasm by ERD6. Monosaccharides in the cytoplasm can also be transported into vacuoles by TMT or VGT.
Figure 2. Various glycotransporters and functions in plants
Phylogenetic analysis found that SWEET and STP were found in prokaryotic and eukaryotic organisms, while SUT was only found in plants and fungi. Glycotransporters rapidly evolve and swell in some plants, suggesting a diversification of functions. In plant-pathogen interactions, plant transporters are antagonistically regulated by plants and pathogens to lead to disease resistance or susceptibility. When the pathogen is a living trophic fungus with a sucker, infection causes STP to absorb monosaccharides into the cell and supply them to the sucker, promoting infection. However, when Lr67res containing STP homologous protein is infected by pathogenic bacteria, the protein loses its function and cannot absorb monosaccharides into cells, resulting in antibacterial properties. When the pathogen is a bacteria, the bacteria secrete TAL effector proteins, up-regulate the expression of SWEET, increase the concentration of sugar excreted outside the cell, and promote the growth of bacteria. Conversely, when flg22 is sensed by plant surface receptors, it excites downstream BAK1 to phosphorylate STP13, promoting the absorption of extracellular sugars, leading to resistance. The dead trophic fungus Rhizoctonia solani can induce the expression of OsSWEET11, resulting in susceptibility; Overexpression of STP13 can increase the effect on dead trophic fungi B. Resistance of the cinera.
Figure 3. The role of glycotransporters in plant-pathogen interactions
In addition to the important role of plant glycotransporters in plant-pathogen interactions, pathogens have evolved the following specific strategies to compete for plant-derived sugars using glycotransporters and glycosinvertases: increasing competition for sugars with high affinity with substrates; Interference with plant sugar partitioning by glycinvertase; Use rare sugars as substrates to avoid direct competition.
Some progress has been made in resistance breeding using existing knowledge of the role of glycotransporters in plant pathogen interactions. There are three main types: disease resistance by restricting the supply of pathogenic glycogens through the constant genetic modification of glycotransporters; Restriction of glycogen supply by specific spatiotemporal-dependent genetically modified glycotransporters to produce disease resistance; Disease resistance is created by limiting the supply of pathogenic glycogens by screening naturally varying transporters. Each of these strategies has its own advantages and disadvantages, and the fundamental problem is to resolve the conflict between plant disease resistance and plant growth.
Plants have evolved a variety of strategies to resist pathogens, on the one hand, by identifying pathogens and activating plant immune responses to eliminate pathogens; On the other hand, by cutting off the nutrient supply of pathogenic bacteria, starvation of pathogens leads to resistance. Merging the two strategies may give us new opportunities to develop more durable and effective resistant plants.
Prof. Xiaokun Liu from Lushan Botanical Garden is the corresponding author, Dr. Chen Yi from the John Innas Center is the first author, Professor Tony Miller from the John Innas Center, Bowen Qiu from the Lushan Botanical Garden, Yao Huang from Nanchang University, Dr. Kai Zhang from the Third Institute of Oceanography in Xiamen, and Dr. Gaili Fan from the Xiamen Greening Center participated in the study. The research was supported by the Natural Science Foundation of Jiangxi Province, the Jiujiang Science and Natural Science Foundation of Jiangxi Province, and the Long-term Project of Innovation Leading Talents of the Thousand Talents Program of Jiangxi Province.
Original link:
https://onlinelibrary.wiley.com/doi/full/10.1111/pbi.14408
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