21st Century Guidebook to Fungi, SECOND EDITION, by David Moore, Geoffrey D. Robson and Anthony P. J. Trinci

Table of Contents

1. Chapter 13: Ecosystem mycology: saprotrophs, and mutualisms between plants and fungi
2. Chapter 14: Fungi as pathogens of plants
   1. Fungal diseases and loss of world agricultural production
   2. A few examples of headline crop diseases
   3. The Rice Blast fungus Magnaporthe grisea (Ascomycota)
   4. Armillaria (Basidiomycota)
   5. Pathogens that produce haustoria (Ascomycota and Basidiomycota)
   6. Cercospora (Ascomycota)
   7. Ophiostoma (Ceratocystis) novo-ulmi (Dutch Elm disease or DED) (Ascomycota)
   8. Black stem rust (Puccinia graminis f. sp. tritici) threatens global wheat harvest
   9. Plant disease basics: the disease triangle
   10. Necrotrophic and biotrophic pathogens of plants
   11. The effects of pathogens on their hosts
   12. How pathogens attack plants
   13. Host penetration through stomatal openings
   14. Direct penetration of the host cell wall
   15. Enzymatic penetration of the host
   16. Pre-formed and induced defence mechanisms in plants
   17. Genetic variation in pathogens and their hosts: co-evolution of disease systems
   18. Chapter 14 References and further reading
   19. Buy a PDF of Chapter 14
3. Chapter 15: Fungi as symbionts and predators of animals

14.16 Pre-formed and induced defence mechanisms in plants

Plants have evolved many defence mechanisms to protect themselves against pathogens; some are part of structure and chemistry of the plant that are built-in to the healthy plant before infection, which contribute to avoidance or prevention of infection, others are reactions to the presence of the pathogen, though the categories do overlap considerably (Table 3).

Table 3. Pre-formed and induced defence mechanisms in plants
Present in plant prior to infection		Induced as a result of infection
Structural	Chemical	Structural	Chemical
Surface wax	Leaf leachate	Lignification	H2O2 (oxidative burst)
Cuticle, bark	Surface pH	Abscission layer	Phytoalexins
Cell walls (thickness)	Toxins (e.g. phenolic compounds)	Tyloses (formed in response to vascular wilt)	defence response proteins and metabolites
Casparian strip (endodermis)	Enzyme inhibitors (e.g. tannins)	Cork formation	Cork formation
		Hypersensitive response: host cells killed rapidly by triggering programmed cell death

Pre-existing defence structures comprise:

• surface waxes,
• the chemical structure, thickness, and crosslinking of epidermal cell walls and the walls of internal barriers (endodermis),
• the anatomical position of stomata and lenticels, and the disposition of epidermal hairs,
• fungal germination inhibitors on the plant surface or in surface tissues (for example phenolic compounds, like catechol in onion (Allium cepa) bulb scales, or chlorogenic acid in potato epidermis; see Fig. 10).

Defences formed in response to infection comprise:

• histological defences at the tissue level;
• formation of cork layers, or abscission layers (if excising a part of the plant will benefit the rest),
• tyloses which block vascular elements and limit disease spread, and
• deposition of gums (resinous, viscous substances that dry into brittle solids) on/in the cell wall or plant surface.
• defence tactics at the cellular/subcellular level, including:
• concentrating cytoplasmic contents surround the site of infection,
• thickening of the cell wall with the β-glucan callose,
• modification or removal of specific attachment or receptor sites for a pathogen or pathogen-produced toxin,
• release of inhibitors by the plant into its immediate environment (numerous phenolic compounds can be produced by plants, some as initial defences (Fig. 10), some as reactive defences and some persist into the soil as allelochemicals (biomolecules released into the environment that influence the growth and development of neighbouring organisms) (Popa et al., 2008)),
• cell wall reinforcement by deposition of cellulose and lignin, and accumulation of hydroxyproline-rich glycoproteins,
• production of protease inhibitors and lytic enzymes such as chitinase and glucanase (which target the fungal wall),
• production of phytoalexins, which are antimicrobial compounds not found in a healthy plant that increase to antimicrobial concentrations after infection; phytoalexins may be terpenoids, glycosteroids or alkaloids (two examples shown in Fig. 12), though the definition has stretched over the years and now includes all plant-produced chemicals that contribute to disease and/or pest resistance, so many of the compounds to which we have already referred would come into this category; a simple functional definition recognise phytoalexins as compounds that are synthesised de novo and phytoanticipins as pre-formed infection inhibitors, but the distinction is not always obvious (Dixon, 2001). Phytoalexins are toxins to the attacking organism and are highly specific; a phytoalexins active against one pest may not repel a different pest.

Fig. 10. Two phenolic compounds which are pre-formed fungal inhibitors. A, catechol in the scales (thin outer tissues) of the onion bulb (Allium cepa); B, chlorogenic acid (an ester of cinnamic acid) in the epidermis of both the potato tuber and green coffee beans.

 

Fig. 11. Two characteristic phytoalexins. A, pisatin, a phytoalexin from pea (Pisum sativum), is an isoflavonoid compound; some pathogenic strains of the fungus Nectria haematococca produce a pisatin demethylase that detoxifies pisatin. B, wyerone is a furanoacetylene phytoalexin produced in broad bean (or faba bean), Vicia faba; wyerone is so named because it was discovered at the Plant Growth Substance and System Fungicides Unit at Wye College (University of London).

The type of induced resistance we have already described, the hypersensitive response, in which the plant produces ROS and hydrogen peroxide to initiate programmed cell death in infected cells so that compromised cells commit suicide to create a physical barrier against the pathogen, is also called the general short-term response.

Plants have an alternative long-term resistance response. Long-term resistance, also known as systemic acquired resistance (SAR), is a whole-plant resistance response occurring following a localised exposure to a pathogen. It involves communication with the rest of the plant using the hormones jasmonate, ethylene, abscisic acid and the accumulation of endogenous salicylic acid. If the gaseous hormones are released from the injured tissue it is possible for neighbouring plants to take part in the resistance response as well.

Indeed, even herbivores can detect aromatic wound response compounds and view the plant as no longer edible. SAR is effective against a wide range of pathogens and is consequently also called ‘broad spectrum’ resistance. The pathogen-induced SAR signal activates a specific molecular signal transduction pathway associated with the induction of a wide range of pathogenesis-related (or ‘PR’) genes that protect from further pathogen intrusion. These functions include the enzymes needed to synthesise phytoalexins.

The signals from the pathogen that cause these active plant responses are called elicitors, which are simply fungal products detected by the plant that induce defence reac­tions. They may be general elicitors, which are produced by all members of a pathogen group, or race or cultivar-specific elicitors that are pro­duced only by pathogens with a particular genotype. The elicitors are often components, or even parts of components, of the hyphal walls of the pathogen; such as the peptide produced by Cladosporium fulvum (Ascomycota) that induces phytoalexin formation by tomatoes, and the branched glucans of Phytophthora megasperma (Oomycota, kingdom Chromista) that elicit resistance responses when the pathogen infects soya bean (Glycine max).

Updated July, 2019