Trichoderma spp. are free-living fungi that are common in soil and root ecosystems. Recent discoveries show that they are opportunistic, avirulent plant symbionts, as well as being parasites of other fungi. At least some strains establish robust and long-lasting colonizations of root surfaces and penetrate into the epidermis and a few cells below this level. They produce or release a variety of compounds that induce localized or systemic resistance responses, and this explains their lack of pathogenicity to plants. These root-microorganism associations cause substantial changes to the plant proteome and metabolism. Plants are protected from numerous classes of plant pathogen by responses that are similar to systemic acquired resistance and rhizobacteria-induced systemic resistance. Root colonization by Trichoderma spp. also frequently enhances root growth and development, crop productivity, resistance to abiotic stresses and the uptake and use of nutrients.

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Trichoderma species--opportunistic, avirulent plant symbionts.

The human diet contains a great variety of natural mutagens and carcinogens, as well as many natural antimutagens and anticarcinogens. Many of these mutagens and carcinogens may act through the generation of oxygen radicals. Oxygen radicals may also play a major role as endogenous initiators of degenerative processes, such as DNA damage and mutation (and promotion), that may be related to cancer, heart disease, and aging. Dietary intake of natural antioxidants could be an important aspect of the body’s defense mechanism against these agents. Many antioxidants are being identified as anticarcinogens. Characterizing and optimizing such defense systems may be an important part of a strategy of minimizing cancer and other age-related diseases.

https://science.sciencemag.org/content/sci/221/4617/1256.full.pdf

Dietary carcinogens and anticarcinogens Oxygen radicals and degenerative diseases

Systemic acquired resistance (SAR) is a mechanism of induced defense that confers long-lasting protection against a broad spectrum of microorganisms. SAR requires the signal molecule salicylic acid (SA) and is associated with accumulation of pathogenesis-related proteins, which are thought to contribute to resistance. Much progress has been made recently in elucidating the mechanism of SAR. Using the model plant Arabidopsis, it was discovered that the isochorismate pathway is the major source of SA during SAR. In response to SA, the positive regulator protein NPR1 moves to the nucleus where it interacts with TGA transcription factors to induce defense gene expression, thus activating SAR. Exciting new data suggest that the mobile signal for SAR might be a lipid molecule. We discuss the molecular and genetic data that have contributed to our understanding of SAR and present a model describing the sequence of events leading from initial infection to the induction of defense genes.

Systemic acquired resistance

Nonpathogenic rhizobacteria can induce a systemic resistance in plants that is phenotypically similar to pathogen-induced systemic acquired resistance (SAR). Rhizobacteria-mediated induced systemic resistance (ISR) has been demonstrated against fungi, bacteria, and viruses in Arabidopsis, bean, carnation, cucumber, radish, tobacco, and tomato under conditions in which the inducing bacteria and the challenging pathogen remained spatially separated. Bacterial strains differ in their ability to induce resistance in different plant species, and plants show variation in the expression of ISR upon induction by specific bacterial strains. Bacterial determinants of ISR include lipopolysaccharides, siderophores, and salicylic acid (SA). Whereas some of the rhizobacteria induce resistance through the SA-dependent SAR pathway, others do not and require jasmonic acid and ethylene perception by the plant for ISR to develop. No consistent host plant alterations are associated with the induced state, but upon challenge inoculation, resistance responses are accelerated and enhanced. ISR is effective under field conditions and offers a natural mechanism for biological control of plant disease.

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Systemic resistance induced by rhizosphere bacteria

The loss of organic material from the roots provides the energy for the development of active microbial populations in the rhizosphere around the root. Generally, saproptrophs or biotrophs such as mycorrhizal fungi grow in the rhizosphere in response to this carbon loss, but plant pathogens may also develop and infect a susceptible host, resulting in disease. This review examines the microbial interactions that can take place in the rhizosphere and that are involved in biological disease control. The interactions of bacteria used as biocontrol agents of bacterial and fungal plant pathogens, and fungi used as biocontrol agents of protozoan, bacterial and fungal plant pathogens are considered. Whenever possible, modes of action involved in each type of interaction are assessed with particular emphasis on antibiosis, competition, parasitism, and induced resistance. The significance of plant growth promotion and rhizosphere competence in biocontrol is also considered. Multiple microbial interactions involving bacteria and fungi in the rhizosphere are shown to provide enhanced biocontrol in many cases in comparison with biocontrol agents used singly. The extreme complexity of interactions that can occur in the rhizosphere is highlighted and some potential areas for future research in this area are discussed briefly.

/pdf/microbial-interactions-and-biocontrol-in-the-rhizosphere-1erj9kqzek.pdf

Microbial interactions and biocontrol in the rhizosphere

Inoculation of the first true leaf of cucumber with Colletotrichum lagenarium enhanced peroxidase activity in leaf 2. The increased activity was associated, at least in part, with the fastest moving anodic isozymes during polyacrylamide gel electrophoresis. All plant parts and cellular fractions exhibited enhanced peroxidase activity in protected as compared to control plants. Injury of leaf 1 with dry ice neither induced systemic resistance to C. lagenarium nor enhanced peroxidase activity of leaf 2. Inoculation of leaf 1 with C. lagenarium followed by inoculation of leaf 2, 1 week later, elicited a higher degree of protection and higher peroxidase activity in leaf 3 than did single inoculations. Increasing numbers of C. lagenarium lesions on leaf 1 progressively increased peroxidase activity and resistance in leaf 2. Induced resistance was detected 3 to 4 days after inoculation of leaf 1, whereas peroxidase activity increased after the 4th day.

Association of enhanced peroxidase activity with induced systemic resistance of cucumber to Colletotrichum lagenarium

Infection of the first true leaf of cucumber with Colletotrichum lagenarium induces systemic resistance (protection) against subsequent challenge by C. lagenarium or Cladosporium cucumerinum Conidia of C. lagenarium germinated and formed appressoria equally well on isolated epidermal strips from protected and control plants; however, penetration occurred less frequently into epidermal strips from protected plants. Inhibition of penetration was associated with host epidermal cell wall lignification directly under appressoria. Lignification occurred more rapidly and to a greater extent in protected than in control plants. Infection of etiolated seedlings resistant to scab with C. cucumerinum made the seedlings resistant to C. lagenarium, and elicited a rapid lignification of penetrated and adjacent host cells. This lignification reaction in the resistant cultivar was histologically indistinguishable from that at sites of penetration in a systemically protected “susceptible” cultivar challenged with C. cucumerinum. Germination of conidia and frequencies of penetration of C. cucumerinum were similar in protected and control plants, but development of the fungus in lignified tissue was markedly restricted. Coniferyl alcohol, a lignin precursor, was toxic to C. lagenarium and C. cucumerinum when only 0·3 hg were applied to thin-layer bioassay plates. This suggests that it might function as a phytoalexin. Mycelia of C. lagenarium and C. cucumerinum were “lignified” in the presence of coniferyl alcohol, peroxidase and hydrogen peroxide.

Lignification as a mechanism for induced systemic resistance in cucumber

Mycelial extracts from Phytophthora infestans caused necrosis and elicited the accumulation of antimicrobial stress metabolites in potato tubers. A portion of the material with elicitor activity could be extracted from the mycelium by a mixture of chloroform and methanol. The most active elicitors of stress metabolites in these extracts were eicosapentaenoic and arachidonic acids. These fatty acids were found in either free or esterified form in all active fractions of the mycelial extracts.

Eicosapentaenoic and Arachidonic Acids from Phytophthora infestans Elicit Fungitoxic Sesquiterpenes in the Potato.

A clear definition of induced disease resistance is lacking, even though the area has been extensively researched and described. The lack of a precise definition leads to potential confusion on whether an underlying mechanism for biological control is induced resistance. We propose definitions, which were developed at a NATO Advanced Research Workshop on biological control, for induced disease resistance and related terms. These definitions are intended to invoke debate and increase effective communication among investigators of induced resistance.

Proposed definitions related to induced disease resistance

Resistance to plant disease is often specific and metabolites and receptors contributing to this specificity may have specific structures. However, simple, structurally-unrelated compounds induce systemic resistance in unrelated plants to diverse pathogens including fungi, bacteria and viruses. Both resistance and induced systemic resistance (ISR) are associated with the rapid accumulation of the same structurally unrelated putative defense compounds that have diverse functions. It has been suggested that cultivar (race)-specific resistance is initiated by the specific interaction of a pathogen product (or pathogen induced product) and a plant receptor. However, restricted infection by pathogens can result in ISR and many different compounds can cause ISR. It is thus evident that there are both specific and non-specific routes to the master switch for ISR and there may be more than one master switch. Are reactive oxygen species and free radicals regulating the master switch(es) via both routes? It is also evident there are many switches, other than the master switch. Adding to the complexity of resistance and ISR are the observations that different compounds and pathways may mediate different biochemical resistances. Activation of one of the pathways may antagonize or enhance the activation or effectiveness of another. The review will address these complexities and questions and propose directions of research which require high priority. Factors which encourage and suppress the application of ISR in agriculture will also be addressed.

Joseph Kuć

Papers

Association of enhanced peroxidase activity with induced systemic resistance of cucumber to Colletotrichum lagenarium

Lignification as a mechanism for induced systemic resistance in cucumber

Eicosapentaenoic and Arachidonic Acids from Phytophthora infestans Elicit Fungitoxic Sesquiterpenes in the Potato.

Proposed definitions related to induced disease resistance

Concepts and Direction of Induced Systemic Resistance in Plants and its Application