Plants represent a rich source of nutrients for many organisms including bacteria, fungi, protists, insects, and vertebrates. Although lacking an immune system comparable to animals, plants have developed a stunning array of structural, chemical, and protein-based defenses designed to detect invading organisms and stop them before they are able to cause extensive damage. Humans depend almost exclusively on plants for food, and plants provide many important non-food products including wood, dyes, textiles, medicines, cosmetics, soaps, rubber, plastics, inks, and industrial chemicals. Understanding how plants defend themselves from pathogens and herbivores is essential in order to protect our food supply and develop highly disease-resistant plant species. This article introduces the concept of plant disease and provides an overview of some defense mechanisms common among higher plants. A close examination of plant anatomy is presented, as well as some of the ecological relationships that contribute to plant defense and disease resistance. Special care has been taken to illustrate how products used in everyday life are derived from substances produced by plants during defense responses. Disciplines
SummarySurprisingly little is known of the trehalose biosynthetic pathways in pseudomonads, despite the importance of trehalose to protecting cells from environmental stresses such as low water availability. The genome of the foliar pathogen Pseudomonas syringae pv. tomato strain DC3000 contains genes for two trehalose biosynthetic pathways, TreS and TreYZ, and lacks genes for the more common OtsAB pathway. Deletion of either the treS (PSPTO_2760-2762) or treY/treZ (PSPTO_3125-3134) locus eliminated trehalose accumulation and reduced bacterial growth under hyperosmotic conditions. In evaluating the role of trehalose in P. syringae fitness on leaves, we found that a double deletion mutant lacking these loci exhibited poorer survival than the wild type on tomato leaves over a 2-week period in a growth chamber. Similarly, this mutant exhibited reduced survival on leaves of susceptible and resistant cultivars of the host plant tomato and of the non-host plant soybean over a 10-day period in field plots. Thus, the trehalose biosynthetic loci in P. syringae, which are highly conserved among pseudomonads, contributed to DC3000 fitness on leaves, supporting a role for trehalose in P. syringae survival and population maintenance in the phyllosphere.
The physiological mechanisms by which plants limit the growth of bacterial pathogens during gene-for-gene resistance are poorly understood. We characterized early events in the Arabidopsis thaliana-Pseudomonas syringae pathosystem to identify physiological changes for which the kinetics are consistent with bacterial growth restriction. Using a safranine-O dye solution to detect vascular activity, we demonstrated that A. thaliana Col-0 resistance to P. syringae pv. tomato DC3000 cells expressing avrRpm1 involved virtually complete cessation of vascular water movement into the infection site within only 3 h postinoculation (hpi), under the conditions tested. This vascular restriction preceded or was simultaneous with precipitous decreases in photosynthesis, stomatal conductance, and leaf transpiration, with the latter two remaining at detectable levels. Microscopic plant cell death was detected as early as 2 hpi. Interestingly, suppression of bacterial growth during AvrRpm1-mediated resistance was eliminated by physically blocking leaf water loss through the stomata without altering plant cell death and was nearly eliminated by incubating plants at high relative humidity. The majority of the population growth benefit from blocking leaf water loss occurred early after inoculation, i.e., between 4 and 8 hpi. Collectively, these results support a model in which A. thaliana suppresses P. syringae growth during gene-for-gene resistance, at least in part, by coupling restricted vascular flow to the infection site with water loss through partially open stomata; that is, the plants effectively starve the invading bacteria for water.
The foliar pathogen Pseudomonas syringae is a useful model for understanding the role of stress adaptation in leaf colonization. We investigated the mechanistic basis of differences in the osmotolerance of two P. syringae strains, B728a and DC3000. Consistent with its higher survival rates following inoculation onto leaves, B728a exhibited superior osmotolerance over DC3000 and higher rates of uptake of plant-derived osmoprotective compounds. A global transcriptome analysis of B728a and DC3000 following an osmotic upshift demonstrated markedly distinct responses between the strains; B728a showed primarily upregulation of genes, including components of the type VI secretion system (T6SS) and alginate biosynthetic pathways, whereas DC3000 showed no change or repression of orthologous genes, including downregulation of the T3SS. DC3000 uniquely exhibited improved growth upon deletion of the biosynthetic genes for the compatible solute N-acetylglutaminylglutamine amide (NAGGN) in a minimal medium, due possibly to NAGGN synthesis depleting the cellular glutamine pool. Both strains showed osmoreduction of glnA1 expression, suggesting that decreased glutamine synthetase activity contributes to glutamate accumulation as a compatible solute, and both strains showed osmoinduction of 5 of 12 predicted hydrophilins. Collectively, our results demonstrate that the superior epiphytic competence of B728a is consistent with its strong osmotolerance, a proactive response to an osmotic upshift, osmoinduction of alginate synthesis and the T6SS, and resiliency of the T3SS to water limitation, suggesting sustained T3SS expression under the water-limited conditions encountered during leaf colonization.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.