The exocyst subunit Exo70B1 is involved in the immune response of Arabidopsis thaliana to different pathogens and cell death

Components of the vesicle trafficking machinery are central to the immune response in plants. The role of vesicle trafficking during pre-invasive penetration resistance has been well documented. However, emerging evidence also implicates vesicle trafficking in early immune signaling. Here we report that Exo70B1, a subunit of the exocyst complex which mediates early tethering during exocytosis is involved in resistance. We show that exo70B1 mutants display pathogen-specific immuno-compromised phenotypes. We also show that exo70B1 mutants display lesion-mimic cell death, which in combination with the reduced responsiveness to pathogen-associated molecular patterns (PAMPs) results in complex immunity-related phenotypes.     

Set‐point control of RD21 protease activity by AtSerpin1 controls cell death in Arabidopsis

Programmed cell death (PCD) in plants plays a key role in defense response and is promoted by the release of compartmentalized proteases to the cytoplasm. Yet the exact identity and control of these proteases is poorly understood. Serpins are an important group of proteins that uniquely curb the activity of proteases by irreversible inhibition; however, their role in plants remains obscure. Here we show that during cell death the Arabidopsis serpin protease inhibitor, AtSerpin1, exhibits a pro‐survival function by inhibiting its target pro‐death protease, RD21. AtSerpin1 accumulates in the cytoplasm and RD21 accumulates in the vacuole and in endoplasmic reticulum bodies. Elicitors of cell death, including the salicylic acid agonist benzothiadiazole and the fungal toxin oxalic acid, stimulated changes in vacuole permeability as measured by the changes in the distribution of marker dye. Concomitantly, a covalent AtSerpin1–RD21 complex was detected indicative of a change in protease compartmentalization. Furthermore, mutant plants lacking RD21 or plants with AtSerpin1 over‐expression exhibited significantly less elicitor‐stimulated PCD than plants lacking AtSerpin1. The necrotrophic fungi Botrytis cinerea and Sclerotina sclerotiorum secrete oxalic acid as a toxin that stimulates cell death. Consistent with a pro‐death function for RD21 protease, the growth of these necrotrophs was compromised in plants lacking RD21 but accelerated in plants lacking AtSerpin1. The results indicate that AtSerpin1 controls the pro‐death function of compartmentalized protease RD21 by determining a set‐point for its activity and limiting the damage induced during cell death.     

Are green islands red herrings? Significance of green islands in plant interactions with pathogens and pests

The term green island was first used to describe an area of living, green tissue surrounding a site of infection by an obligately biotrophic fungal pathogen, differentiated from neighbouring yellowing, senescent tissue. However, it has now been used to describe symptoms formed in response to necrotrophic fungal pathogens, virus infection and infestation by certain insects. In leaves infected by obligate biotrophs such as rust and powdery mildew pathogens, green islands are areas where senescence is retarded, photosynthetic activity is maintained and polyamines accumulate. We propose such areas, in which both host and pathogen cells are alive, be termed green bionissia. By contrast, we propose that green areas associated with leaf damage caused by toxins produced by necrotrophic fungal pathogens be termed green necronissia. A range of biotrophic/hemibiotrophic fungi and leaf-mining insects produce cytokinins and it has been suggested that this cytokinin secretion may be responsible for the green island formation. Indeed, localised cytokinin accumulation may be a common mechanism responsible for green island formation in interactions of plants with biotrophic fungi, viruses and insects. Models have been developed to study if green island formation is pathogen-mediated or host-mediated. They suggest that green bionissia on leaves infected by biotrophic fungal pathogens represent zones of host tissue, altered physiologically to allow the pathogen maximum access to nutrients early in the interaction, thus supporting early sporulation and increasing pathogen fitness. They lead to the suggestion that green islands are 'red herrings', representing no more than the consequence of the infection process and discrete changes in leaf senescence.     

The novel avirulence effector AlAvr1 from Ascochyta lentis mediates host cultivar specificity of ascochyta blight in lentil

Ascochyta lentis is a fungal pathogen that causes ascochyta blight in the important grain legume species lentil, but little is known about the molecular mechanism of disease or host specificity. We employed a map‐based cloning approach using a biparental A. lentis population to clone the gene AlAvr1‐1 that encodes avirulence towards the lentil cultivar PBA Hurricane XT. The mapping population was produced by mating A. lentis isolate P94‐24, which is pathogenic on the cultivar Nipper and avirulent towards Hurricane, and the isolate AlKewell, which is pathogenic towards Hurricane but not Nipper. Using agroinfiltration, we found that AlAvr1‐1 from the isolate P94‐24 causes necrosis in Hurricane but not in Nipper. The homologous corresponding gene in AlKewell, AlAvr1‐2, encodes a protein with amino acid variation at 23 sites and four of these sites have been positively selected in the P94‐24 branch of the phylogeny. Loss of AlAvr1‐1 in a gene knockout experiment produced a P94‐24 mutant strain that is virulent on Hurricane. Deletion of AlAvr1‐2 in AlKewell led to reduced pathogenicity on Hurricane, suggesting that the gene may contribute to disease in Hurricane. Deletion of AlAvr1‐2 did not affect virulence for Nipper and AlAvr1‐2 is therefore not an avirulence gene for Nipper. We conclude that the hemibiotrophic pathogen A. lentis has an avirulence effector, AlAvr1‐1, that triggers a hypersensitive resistance response in Hurricane. This is the first avirulence gene to be characterized in a legume pathogen from the Pleosporales and may help progress research on other damaging Ascochyta pathogens.     

Fusarium oxysporum hijacks COI1-mediated jasmonate signaling to promote disease development in Arabidopsis

Although defense responses mediated by the plant oxylipin jasmonic acid (JA) are often necessary for resistance against pathogens with necrotrophic lifestyles, in this report we demonstrate that jasmonate signaling mediated through COI1 in Arabidopsis thaliana is responsible for susceptibility to wilt disease caused by the root-infecting fungal pathogen Fusarium oxysporum . Despite compromised JA-dependent defense responses, the JA perception mutant coronatine insensitive 1 ( coi1 ), but not JA biosynthesis mutants, exhibited a high level of resistance to wilt disease caused by F. oxysporum . This response was independent from salicylic acid-dependent defenses, as coi1/NahG plants showed similar disease resistance to coi1 plants. Inoculation of reciprocal grafts made between coi1 and wild-type plants revealed that coi1 -mediated resistance occurred primarily through the coi1 rootstock tissues. Furthermore, microscopy and quantification of fungal DNA during infection indicated that coi1 -mediated resistance was not associated with reduced fungal penetration and colonization until a late stage of infection, when leaf necrosis was highly developed in wild-type plants. In contrast to wild-type leaves, coi1 leaves showed no necrosis following the application of F. oxysporum culture filtrate, and showed reduced expression of senescence-associated genes during disease development, suggesting that coi1 resistance is most likely achieved through the inhibition of F. oxysporum -incited lesion development and plant senescence. Together, our results indicate that F. oxysporum hijacks non-defensive aspects of the JA-signaling pathway to cause wilt-disease symptoms that lead to plant death in Arabidopsis.