An Elicitor from Botrytis cinerea Induces the Hypersensitive Response in Arabidopsis thaliana and Other Plants and Promotes the Gray Mold Disease

Abstract

Botrytis cinerea is a necrotrophic fungus that infects over 200 plant species. Previous studies showed that host cells collapse in advance of the hyphae, suggesting secretion of toxins or elicitors. We have partially characterized elicitor activity from intercellular fluid extracted from Arabidopsis thaliana leaves infected with B. cinerea. Treatment of intact leaves or cell cultures with either intercellular fluid from infected leaves or medium from inoculated A. thaliana cell culture induced generation of reactive oxygen species, resulting in reduced photosynthesis, electrolyte leakage, and necrotic lesions that resembled the hypersensitive response (HR). The necrosis was inhibited by diphenyleneiodonium, a specific inhibitor of NADPH oxidase, and by chelating free iron, suggesting the involvement of hydroxyl radicals. The necrosis was also suppressed in dnd1 mutants that are compromised in HR. In contrast, increased cell death was observed in acd2 mutants, indicating the involvement of the host defense signaling pathways. Treatment with the intercellular fluid from infected leaves also induced transcription of pathogenesis-related (PR) genes, such as PR-1, PR-5, HSR203J, and of senescence-associated gene SAG-13. Moreover, rapid transcription of the ethylene-dependent AtEBP gene was detected, indicating induction of ethylene production. The inter-cellular fluid from infected A. thaliana induced cell death in other plants, in line with the lack of B. cinerea specificity. In summary, the intercellular fluid mimicked a range of molecular and physiological host responses that are observed during infection with a live fungus. Moreover, it accelerated the B. cinerea infection, suggesting that the elicitor may act as a pathogenicity factor in the progression of gray mold disease.

Arabidopsis Cell Death in Compatible and Incompatible Interactions with Alternaria brassicicola

“…Altered PCD regulation by these mutations is able to change the host-pathogen interactions. Infiltration of the intercellular fluid from B. cinerea-infected Arabidopsis plants provoked more rapid and actively enlarged necrosis in acd2 (Asai et al, 2000;Govrin et al, 2006). However, the same treatment did not trigger observable alterations in dnd1.…”

Resistance to Botrytis cinerea in sitiens, an Abscisic Acid-Deficient Tomato Mutant, Involves Timely Production of Hydrogen Peroxide and Cell Wall Modifications in the Epidermis

“…B. cinerea induces ROS formation in plants, resulting in hypersensitive cell death that facilitates fungal colonization (Elad, 1992;von Tiedemann, 1997;Govrin and Levine, 2000;Schouten et al, 2002;Govrin et al, 2006). We propose that timing, localization, and function of the increase in ROS are crucial in its role on B. cinerea development.…”

Arabidopsis root K+-efflux conductance activated by hydroxyl radicals: single-channel properties, genetic basis and involvement in stress-induced cell death

“…Notably, both HR production and K + leakage have been observed in plants treated with other pathogenic elicitors, originating, for example, from Botrytis cinerea (Govrin et al, 2006), Alternaria alternate (Jennings et al, 2002) and Magnaporthe grisea (Pasechnik et al, 1998). In these cases, however, K + -channel activation was not characterised.…”