Roles of iron in plant defence and fungal virulence.

University of Saskatchewan
Plant signaling & behavior 08/2007; 2(4):300-2. DOI: 10.4161/psb.2.4.4042
Source: PubMed

ABSTRACT Iron is an essential component of various proteins and pigments for both plants and pathogenic fungi. However, redox cycling between the ferric and ferrous forms of iron can also catalyse the production of dangerous free radicals and iron homeostasis is therefore tightly regulated. our work has indicated that monocot plants challenged by pathogenic fungi redistribute cellular iron to the apoplast in a controlled manner to activate both intracellular and extracellular defences. In the apoplast, the accumulation of free, reactive ferric iron mediates defensive H(2)O(2) production. Inside the cell, this efflux of iron creates a state of iron depletion, which directs the transcription of pathogenesis-related genes in concert with H(2)O(2). In this addendum, we describe differences between the roles of iron in mediation of the oxidative burst in cereal and Arabidopsis responses to fungal pathogens. Also, we discuss the implications of current work concerning fungal iron uptake on host defence strategies.

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    ABSTRACT: Iron (Fe) is an essential element for plant pathogens as well as for their host plants. Since Fe plays a central role in pathogen virulence, most plants have evolved Fe-withholding strategies to reduce Fe availability to pathogens. On the other hand, plants need Fe for an oxidative burst in their basal defense response against pathogens. To investigate how the plant Fe nutritional status affects plant tolerance to a hemibiotrophic fungal pathogen, we employed the maize-Colletotrichum graminicola pathosystem. Fungal infection progressed rapidly via biotrophic to necrotrophic growth in Fe-deficient leaves, while an adequate Fe nutritional status suppressed the formation of infection structures of C. graminicola already during the early biotrophic growth phase. As indicated by Prussian blue and DAB staining, the retarding effect of an adequate Fe nutritional status on fungal development coincided temporally and spatially with the recruitment of Fe to infection sites and a local production of H2 O2 . A similar coincidence between local Fe and H2 O2 accumulation was found in a parallel approach employing C. graminicola mutants affected in Fe acquisition and differing in virulence. These results indicate that an adequate Fe nutritional status delays and partially suppresses the fungal infection process and the biotrophic growth phase of C. graminicola, most likely via the recruitment of free Fe to the fungal infection site for a timely oxidative burst.
    Physiologia Plantarum 02/2014; · 3.26 Impact Factor
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    ABSTRACT: The present study aimed to determine the most efficient experimental conditions of iron sulfate use leading to optimal inhibition in the development of fungal pathogens. Assays have been focused on fungal species inducing severe grapevine diseases. FeSO4 directly inhibited the in vitro mycelial growth of Botrytis cinerea, Eutypa lata, Phaeomoniella chlamydospora, Phaeoacremonium aleophilum, Diplodia seriata, and Neofusicoccum parvum with variable efficiency in the range of 0.5–10mM. The development was always completely inhibited at 20mM. This inhibitory effect was greatly increased at acidic pH values. The anionic moiety of the molecule was of importance since bromide, chloride and sulfate were highly active, whereas acetate and oxalate showed a small effect. Electron microscope observations on E. lata and B. cinerea showed that a treatment with FeSO4 induced dramatic changes in the hyphal organization leading to cell death. No toxicity was observed on grapevine leaves following repeated FeSO4 sprays in the antifungal concentration range. Therefore, FeSO4 may be proposed to effectively replace the long-term pollutant use of CuSO4 as an antifungal agent, with the additional advantage of iron being an important plant micronutrient.
    Scientia Horticulturae 09/2011; 130(3):517-523. · 1.50 Impact Factor


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