Necrotroph attacks on plants: wanton destruction or covert extortion?

Abstract

Necrotrophic pathogens cause major pre- and post-harvest diseases in numerous agronomic and horticultural crops inflicting significant economic losses. In contrast to biotrophs, obligate plant parasites that infect and feed on living cells, necrotrophs promote the destruction of host cells to feed on their contents. This difference underpins the divergent pathogenesis strategies and plant immune responses to biotrophic and necrotrophic infections. This chapter focuses on Arabidopsis immunity to necrotrophic pathogens. The strategies of infection, virulence and suppression of host defenses recruited by necrotrophs and the variation in host resistance mechanisms are highlighted. The multiplicity of intraspecific virulence factors and species diversity in necrotrophic organisms corresponds to variations in host resistance strategies. Resistance to host-specific necrotophs is monogenic whereas defense against broad host necrotrophs is complex, requiring the involvement of many genes and pathways for full resistance. Mechanisms and components of immunity such as the role of plant hormones, secondary metabolites, and pathogenesis proteins are presented. We will discuss the current state of knowledge of Arabidopsis immune responses to necrotrophic pathogens, the interactions of these responses with other defense pathways, and contemplate on the directions of future research.

Figure 1.

B. cinerea resistance in Arabidopsis transgenic CUTE plants expressing a Fusarium pisi cutinase gene. Images show fungal growth as revealed by trypan blue staining at 12–48 h after inoculation (Pictures are courtesy of Jean-Pierre Metraux. University of Fribourg, Switzerland).

Figure 2.

Arabidopsis wound-induced immunity to B. cinerea. Fungal growth in plants inoculated with B. cinerea with and without wounding as revealed with trypan blue staining. hpi, hours after inoculation. (Pictures are courtesy of Jean-Pierre Metraux, University of Fribourg, Switzerland)

Figure 3.

B. cinerea disease symptoms in wild type (Col-0) Arabidopsis B. cinerea causes necrotic lesions on a wild type Arabidopsis. Images show progress of typical disease symptom from 1 to 4 dpi. Plants were sprayed with 2.5 × 10⁵ spores/ml B. cinerea suspension. dpi, days post infection.

Figure 4.

Disease symptoms in wild type (Col-0) and bik1 mutant plants after spray-inoculation with a B. cinerea conidial suspension (2.5×10⁵ spores/ml). Sites of infection are clearly visible as restricted necrotic sites in the wild type plants. The bik1 plants show enhanced chlorosis as an early disease symptom.

Figure 5.

Disease symptoms in wild type (Col-0), and (A) bos1 and, (C) bos3 mutant plants after spray-inoculation with a B. cinerea conidial suspension (2.5×10⁵ spores/ml). The RNA-blot in (B) shows accumulation of the B. cinerea Tublin A gene transcript as a measure of fungal growth. The bos3 plants show increased necrosis and chlorosis after inoculation with B. cinerea. d, days after inoculation.

Figure 6.

Progress of disease symptom in wild type, wrky33 and 35S:WRKY33 plants sprayed with 2.5 × 10⁵ spores/ml B. cinerea suspension.

Figure 7.

Disease symptoms caused by Alternaria brassicicola in Arabidopsis wild type, hub1 and 35S:HUB1 plants. (A) Detached leaves were drop-inoculated (5 µl, 5×10⁵ spores/ml). (B) Disease symptoms and measurements of fungal growth are from 5 dpi. dpi, days post infection.