The innate immune system is a host defense mechanism that is evolutionarily conserved from insects to human and is mainly involved in the recognition and control of the early stage of infection in all animals (1). Over the last decade, it has become increasingly evident that also plants have acquired the ability to recognize "non self" via sensitive perception systems for components of microorganisms called pathogen-associated molecular patterns (PAMPs) 2 (2-4). As classically defined, PAMPs are highly characteristic of potentially infectious microbes, but are not present in the host. In addition, such patterns are often vital for microbial survival and are therefore not subject to mutational variation. PAMPs that trigger innate immune responses in various vertebrate and non-vertebrate organisms include lipopolysaccharides (LPS) from Gram-negative bacteria, eubacterial flagellin, viral, and bacterial nucleic acids, fungal cell wall-derived glucans, chitins, mannans, or proteins and peptidoglycans (PGN) from Gram-positive bacteria (5-8). Peptidoglycan (PGN) is an essential and unique component of the bacterial envelope that provides rigidity and structure to the bacterial cell. Virtually all bacteria contain a layer of PGN, but the amount, location, and specific composition vary. PGN is a polymer of alternating N-acetylglucosamine (GlcNAc) and N-acetyl-muramic acid (MurNAc) residues in -1-4 linkage which are cross-linked by short peptides (9, 10). The glycan chains display little variation among different bacterial species while the peptide subunit and the interpeptide bridge reveal species specific differences. PGN from Staphylococcus aureus belongs to the L-lysine (Lys)-type, which is primarily found in Gram-positive bacteria whereas meso-diaminopimelate (Dap)-type PGN is typical for many Gram-negative bacteria.As PGNs are located on most bacterial surfaces they constitute excellent targets for recognition by the innate immune system. Indeed, PGN is known for a long time to promote an innate immune response in vertebrates and insects (11-13), and a breakdown product of PGN, muramyl dipeptide (MurNAc-L-Ala-D-Glu; MDP) was found to be the minimal chemical structure required for PAMP activity in mammals (14). PGN is perceived in animals via various pattern recognition receptors (PRRs), including scavenger receptors, nucleotide-binding oligomerization domain-containing proteins (NODs), a family of peptidoglycan recognition proteins (PGRPs), PGN-lytic enzymes and Toll-like receptor TLR2 (15-19).Remarkable similarities have been uncovered in the molecular mode of PAMP perception in animals and plants (2,20,21). Perception of flagellin in Arabidopsis was shown to be depend-* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
SUMMARYIn plants, autophagy has been assigned 'pro-death' and 'pro-survival' roles in controlling programmed cell death associated with microbial effector-triggered immunity. The role of autophagy in basal immunity to virulent pathogens has not been addressed systematically, however. Using several autophagy-deficient (atg) genotypes, we determined the function of autophagy in basal plant immunity. Arabidopsis mutants lacking ATG5, ATG10 and ATG18a develop spreading necrosis upon infection with the necrotrophic fungal pathogen, Alternaria brassicicola, which is accompanied by the production of reactive oxygen intermediates and by enhanced hyphal growth. Likewise, treatment with the fungal toxin fumonisin B1 causes spreading lesion formation in atg mutant genotypes. We suggest that autophagy constitutes a 'pro-survival' mechanism that controls the containment of host tissue-destructive microbial infections. In contrast, atg plants do not show spreading necrosis, but exhibit marked resistance against the virulent biotrophic phytopathogen, Pseudomonas syringae pv. tomato. Inducible defenses associated with basal plant immunity, such as callose production or mitogen-activated protein kinase activation, were unaltered in atg genotypes. However, phytohormone analysis revealed that salicylic acid (SA) levels in non-infected and bacteria-infected atg plants were slightly higher than those in Col-0 plants, and were accompanied by elevated SA-dependent gene expression and camalexin production. This suggests that previously undetected moderate infection-induced rises in SA result in measurably enhanced bacterial resistance, and that autophagy negatively controls SA-dependent defenses and basal immunity to bacterial infection. We infer that the way in which autophagy contributes to plant immunity to different pathogens is mechanistically diverse, and thus resembles the complex role of this process in animal innate immunity.
Abstract:Since its first identification in Poland in 2006, the ascomycete Hymenoscyphus fraxineus has caused massive dieback of Fraxinus excelsior in the countries of eastern, northern and central Europe. This work shows the development, expansion, and severity of the disease in south-eastern Germany for a period of four years, starting in 2010. Differences between habitats, as well as age classes have been captured. The presence and the amount of potentially resistant trees were proven over the years, to determine how high the resistance level might be. Typical disease symptoms are the wilting of leaves, necrotic lesions in the bark and reddish discolorations of branches and stems. In addition, stem necroses also appear by infection with species of Armillaria. Therefore, special attention has been given to Armillaria species in affected ash stands but also to other secondary pathogens, like ash bark beetles. It is shown that breeding galleries of Hylesinus fraxini are only found in trees that have recently died and thus Hylesinus fraxini is still acting as a secondary opportunistic pathogen. In contrast, Armillaria spp. can be considered as serious pathogens of weakened ash trees. In different ash stands, typical symptoms of infection can be found. A relationship between stem base necrotic lesions and vitality was examined. It is shown that necrotic lesions severely contribute to accelerating the mortality of ash trees. In addition to the high infection pressure by H. fraxineus, the high inoculum of Armillaria in the soil facilitates further infections and, thus, likewise endangers the survival of potentially resistant trees. In the following years, forest conversion and seed harvest in affected ash stands will have to be urgently considered to avoid tree gaps on a large scale. Furthermore, infection assays of potentially resistant trees with ensuing breeding programmes should be initially started for the conservation of this ecologically and economically important tree species.
A utophagy has an important function in cellular homeostasis. In recent years autophagy has been implicated in plant basal immunity and assigned negative ("anti-death") and positive ("pro-death") regulatory functions in controlling cell death programs that establish sufficient immunity to microbial infection. We recently showed that Arabidopsis mutants lacking the autophagy-associated (ATG) genes ATG5, ATG10 and ATG18a are compromised in their resistance towards infection with necrotrophic fungal pathogens but display an enhanced resistance towards biotrophic bacterial invaders. Thus, the function of autophagy as either being pro-death or anti-death depends critically on the lifestyle and infection strategy of invading microbes. Here we show that ATG7 contributes to resistance to fungal pathogens. Genetic inactivation of ATG7 results in elevated susceptibility towards the necrotrophic fungal pathogen, Alternaria brassicicola, with atg7 mutants developing spreading necrosis accompanied by production of reactive oxygen intermediates. Likewise, treatment with the fungal toxin fumonisin B1 causes spreading lesion formation in the atg7 mutant. We conclude that ATG7-dependent autophagy constitutes an "anti-death" ("pro-survival") plant mechanism to control the containment of cell death and immunity to necrophic fungal infection.Plants have evolved a bipartite plant immune system to cope with microbial infections. The first layer of defense relies on the recognition of pathogenassociated molecular patterns (PAMP)
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