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Callose deposition at plasmodesmata is a critical factor in restricting the cell-to-cell movement of Soybean mosaic virus.

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Callose is a β-l,3-glucan with diverse roles in the viral pathogenesis of plants. It is widely believed that the deposition of callose and hypersensitive reaction (HR) are critical defence responses of host plants against viral infection. However, the sequence of these two events and their

Abscisic acid is involved in chitosan-induced resistance to tobacco necrosis virus (TNV).

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Chitosan (CHT) antiviral activity has been further investigated in the pathosystem Phaseolus vulgaris - tobacco necrosis virus (TNV). CHT application elicited both callose apposition and ABA accumulation in leaf tissues, at 12 and 24h after treatment, respectively, and induced a high level of

HCPro suppression of callose deposition contributes to strain specific resistance against Potato virus Y.

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Potato virus Y (PVY, Potyviridae) is a continuing challenge for potato production due to the increasing popularity of strain-specific resistant cultivars. Hypersensitive resistance (HR) is one type of plant defense response to restrict virus spread. In many potato cultivars, such as cv Premier

In spite of induced multiple defense responses, tomato plants infected with Cucumber mosaic virus and D satellite RNA succumb to systemic necrosis.

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Cucumber mosaic virus (CMV) D satellite RNA (satRNA) attenuates the symptoms induced by CMV in most plants, but causes leaf epinasty and systemic necrosis in tomato plants, where programmed cell death (PCD) is involved. However, our understanding of the cellular and molecular responses to the

A family of conserved bacterial effectors inhibits salicylic acid-mediated basal immunity and promotes disease necrosis in plants.

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Salicylic acid (SA)-mediated host immunity plays a central role in combating microbial pathogens in plants. Inactivation of SA-mediated immunity, therefore, would be a critical step in the evolution of a successful plant pathogen. It is known that mutations in conserved effector loci (CEL) in the

Pathogen development and host responses to Plasmopara viticola in resistant and susceptible grapevines: an ultrastructural study.

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The downy mildew disease in grapevines is caused by Plasmopara viticola. This disease poses a serious threat wherever viticulture is practiced. Wild Vitis species showing resistance to P. viticola offer a promising pathway to develop new grapevine cultivars resistant to P. viticola which will allow

DspA/E, a type III effector essential for Erwinia amylovora pathogenicity and growth in planta, induces cell death in host apple and nonhost tobacco plants.

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Erwinia amylovora is responsible for fire blight, a necrotic disease of apples and pears. E. amylovora relies on a type III secretion system (TTSS) to induce disease on hosts and hypersensitive response (HR) on nonhost plants. The DspA/E protein is essential for E. amylovora pathogenicity and is

Ultrastructure of the Penetration and Infection of Pansy Roots by Thielaviopsis basicola.

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ABSTRACT Transmission electron microscopy was used to study the penetration and infection of pansy roots by Thielaviopsis basicola. Events observed in 7- to 10-day-old roots produced on moist filter paper differed slightly from those in roots from 4-week-old plants washed free of potting media prior

Two host cytoplasmic effectors are required for pathogenesis of Phytophthora sojae by suppression of host defenses.

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Phytophthora sojae encodes hundreds of putative host cytoplasmic effectors with conserved FLAK motifs following signal peptides, termed crinkling- and necrosis-inducing proteins (CRN) or Crinkler. Their functions and mechanisms in pathogenesis are mostly unknown. Here, we identify a group of five P.

Looking inside phytoplasma-infected sieve elements: A combined microscopy approach using Arabidopsis thaliana as a model plant.

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Phytoplasmas are phloem-inhabiting plant pathogens that affect over one thousand plant species, representing a severe threat to agriculture. The absence of an effective curative strategy and the economic importance of many affected crops make a priority of studying how plants respond to phytoplasma

NPP1, a Phytophthora-associated trigger of plant defense in parsley and Arabidopsis.

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Activation of non-cultivar-specific plant defense against attempted microbial infection is mediated through the recognition of pathogen-derived elicitors. Previously, we have identified a peptide fragment (Pep-13) within a 42-kDa cell wall transglutaminase from various Phytophthora species that

Phytotoxicity and innate immune responses induced by Nep1-like proteins.

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We show that oomycete-derived Nep1 (for necrosis and ethylene-inducing peptide1)-like proteins (NLPs) trigger a comprehensive immune response in Arabidopsis thaliana, comprising posttranslational activation of mitogen-activated protein kinase activity, deposition of callose, production of nitric

Dissecting the beta-aminobutyric acid-induced priming phenomenon in Arabidopsis.

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Plants treated with the nonprotein amino acid beta-aminobutyric acid (BABA) develop an enhanced capacity to resist biotic and abiotic stresses. This BABA-induced resistance (BABA-IR) is associated with an augmented capacity to express basal defense responses, a phenomenon known as priming. Based on

Autophagy differentially controls plant basal immunity to biotrophic and necrotrophic pathogens.

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In 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

Phenotypic and histochemical traits of the interaction between Plasmopara viticola and resistant or susceptible grapevine varieties.

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BACKGROUND Grapevine downy mildew, caused by Plasmopara viticola, is a very serious disease affecting mainly Vitis vinifera cultivated varieties around the world. Breeding for resistance through the crossing with less susceptible species is one of the possible means to reduce the disease incidence

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