Licensed to kill: the lifestyle of a necrotrophic plant pathogen
TL;DR: Targeted mutagenesis studies are unraveling the roles played in the infection process by a variety of B. cinerea genes that are required for penetration, host cell killing, plant tissue decomposition or signaling.
About: This article is published in Trends in Plant Science.The article was published on 2006-05-01. It has received 597 citations till now. The article focuses on the topics: Botrytis cinerea.
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TL;DR: New evidence suggests that the pathogen triggers the host to induce programmed cell death as an attack strategy, which could offer new approaches for stable polygenic resistance in future.
Abstract: Introduction: Botrytis cinerea (teleomorph: Botryotinia fuckeliana) is an airborne plant pathogen with a necrotrophic lifestyle attacking over 200 crop hosts worldwide. Although there are fungicides for its control, many classes of fungicides have failed due to its genetic plasticity. It has become an important model for molecular study of necrotrophic fungi. Taxonomy: Kingdom: Fungi, phylum: Ascomycota, subphylum: Pezizomycotina, class: Leotiomycetes, order: Helotiales, family: Sclerotiniaceae, genus: Botryotinia. Host range and symptoms: Over 200 mainly dicotyledonous plant species, including important protein, oil, fibre and horticultural crops, are affected in temperate and subtropical regions. It can cause soft rotting of all aerial plant parts, and rotting of vegetables, fruits and flowers post-harvest to produce prolific grey conidiophores and (macro)conidia typical of the disease. Pathogenicity: B. cinerea produces a range of cell-wall-degrading enzymes, toxins and other low-molecular-weight compounds such as oxalic acid. New evidence suggests that the pathogen triggers the host to induce programmed cell death as an attack strategy. Resistance: There are few examples of robust genetic host resistance, but recent work has identified quantitative trait loci in tomato that offer new approaches for stable polygenic resistance in future.
1,199 citations
TL;DR: Current knowledge about the phloem transport mechanisms is summarized and the effects of several abiotic (water and salt stress, mineral deficiency, CO2, light, temperature, air, and soil pollutants) and biotic andmutualistic and pathogenic microbes, viruses, aphids, and parasitic plants are reviewed.
Abstract: Source-to-sink transport of sugar is one of the major determinants of plant growth and relies on the efficient and controlled distribution of sucrose (and some other sugars such as raffinose and polyols) across plant organs through the phloem. However, sugar transport through the phloem can be affected by many environmental factors that alter source/sink relationships. In this paper, we summarize current knowledge about the phloem transport mechanisms and review the effects of several abiotic (water and salt stress, mineral deficiency, CO2, light, temperature, air, and soil pollutants) and biotic (mutualistic and pathogenic microbes, viruses, aphids, and parasitic plants) factors. Concerning abiotic constraints, alteration of the distribution of sugar among sinks is often reported, with some sinks as roots favored in case of mineral deficiency. Many of these constraints impair the transport function of the phloem but the exact mechanisms are far from being completely known. Phloem integrity can be disrupted (e.g., by callose deposition) and under certain conditions, phloem transport is affected, earlier than photosynthesis. Photosynthesis inhibition could result from the increase in sugar concentration due to phloem transport decrease. Biotic interactions (aphids, fungi, viruses…) also affect crop plant productivity. Recent breakthroughs have identified some of the sugar transporters involved in these interactions on the host and pathogen sides. The different data are discussed in relation to the phloem transport pathways. When possible, the link with current knowledge on the pathways at the molecular level will be highlighted.
852 citations
Cites background from "Licensed to kill: the lifestyle of ..."
...In contrast, necrotrophic pathogens secrete toxins and produce hydrolytic enzymes that kill host cells in order to feed on macerating tissues (van Kan, 2006)....
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TL;DR: The controversial evidence pointing to either a repression or a promotion of resistance by ABA is discussed and a model in which both possibilities are integrated is proposed.
720 citations
Cites background from "Licensed to kill: the lifestyle of ..."
...the first pre-invasive defense barrier of the plant (Phase I). Some fungal and oomycete pathogens can penetrate the cell wall directly, whereas others enter the tissue through natural openings, such as stomata or wounds [6, 7 ]....
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...Some fungi overcome the first cell layer by applying mechanical force onto the epidermal cell wall or by secreting cuticle- and cell-wall-degrading enzymes [6, 7 ]....
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TL;DR: This review specifically focuses on these pathogenesis-related peptides, including proteinase inhibitors, plant defensins, thionins,Thionins and lipid transfer proteins, including novel peptide families, including PR-6 family, which are identified during the last decade.
656 citations
TL;DR: It is proposed that a new generation of genetic resources, complemented by careful phenotypic analysis, will produce a deeper understanding of plant defense and more effective utilization of natural resistance alleles.
615 citations
References
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TL;DR: Genome-wide analysis of the distribution of integration events revealed the existence of a large integration site bias at both the chromosome and gene levels, and insertion mutations were identified in genes that are regulated in response to the plant hormone ethylene.
Abstract: Over 225,000 independent Agrobacterium transferred DNA (T-DNA) insertion events in the genome of the reference plant Arabidopsis thaliana have been created that represent near saturation of the gene space. The precise locations were determined for more than 88,000 T-DNA insertions, which resulted in the identification of mutations in more than 21,700 of the approximately 29,454 predicted Arabidopsis genes. Genome-wide analysis of the distribution of integration events revealed the existence of a large integration site bias at both the chromosome and gene levels. Insertion mutations were identified in genes that are regulated in response to the plant hormone ethylene.
5,227 citations
"Licensed to kill: the lifestyle of ..." refers background in this paper
...mutants can be generated, just as in Arabidopsis [ 71 ], and screened phenotypically....
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TL;DR: The draft sequence of the M. grisea genome is reported, reflecting the clonal nature of this fungus imposed by widespread rice cultivation and analysis of the gene set provides an insight into the adaptations required by a fungus to cause disease.
Abstract: Magnaporthe grisea is the most destructive pathogen of rice worldwide and the principal model organism for elucidating the molecular basis of fungal disease of plants. Here, we report the draft sequence of the M. grisea genome. Analysis of the gene set provides an insight into the adaptations required by a fungus to cause disease. The genome encodes a large and diverse set of secreted proteins, including those defined by unusual carbohydrate-binding domains. This fungus also possesses an expanded family of G-protein-coupled receptors, several new virulence-associated genes and large suites of enzymes involved in secondary metabolism. Consistent with a role in fungal pathogenesis, the expression of several of these genes is upregulated during the early stages of infection-related development. The M. grisea genome has been subject to invasion and proliferation of active transposable elements, reflecting the clonal nature of this fungus imposed by widespread rice cultivation.
1,520 citations
"Licensed to kill: the lifestyle of ..." refers background in this paper
...However, the genome sequence of B. cinerea appears to contain at least five additional cutinase genes and over a dozen lipase genes, as is also the case in M. grisea [ 18 ]....
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TL;DR: It is shown that, although hypersensitive cell death is efficient against biotrophic pathogens, it does not protect plants against infection by the necrotrophic pathogens B. cinerea and S. sclerotiorum.
1,081 citations
TL;DR: This review summarizes current knowledge of mechanisms employed by the fungus to parasitize its host with emphasis on biology, physiology and molecular aspects of pathogenicity.
Abstract: Sclerotinia sclerotiorum (Lib.) de Bary is a necrotrophic fungal pathogen causing disease in a wide range of plants. This review summarizes current knowledge of mechanisms employed by the fungus to parasitize its host with emphasis on biology, physiology and molecular aspects of pathogenicity. In addition, current tools for research and strategies to combat S. sclerotiorum are discussed. Taxonomy: Sclerotinia sclerotiorum (Lib.) de Bary: kingdom Fungi, phylum Ascomycota, class Discomycetes, order Helotiales, family Sclerotiniaceae, genus Sclerotinia. Identification: Hyphae are hyaline, septate, branched and multinucleate. Mycelium may appear white to tan in culture and in planta. No asexual conidia are produced. Long-term survival is mediated through the sclerotium; a pigmented, multi-hyphal structure that can remain viable over long periods of time under unfavourable conditions for growth. Sclerotia can germinate to produce mycelia or apothecia depending on environmental conditions. Apothecia produce ascospores, which are the primary means of infection in most host plants. Host range: S. sclerotiorum is capable of colonizing over 400 plant species found worldwide. The majority of these species are dicotyledonous, although a number of agriculturally significant monocotyledonous plants are also hosts. Disease symptoms: Leaves usually have water-soaked lesions that expand rapidly and move down the petiole into the stem. Infected stems of some species will first develop dark lesions whereas the initial indication in other hosts is the appearance of water-soaked stem lesions. Lesions usually develop into necrotic tissues that subsequently develop patches of fluffy white mycelium, often with sclerotia, which is the most obvious sign of plants infected with S. sclerotiorum.
866 citations
"Licensed to kill: the lifestyle of ..." refers background in this paper
...Two reviews about the infection strategies of S. sclerotiorum have been published recently [6, 7 ]....
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