L.21-G.Biology Mycology D.Ebtihal Muiz

Plant Diseases caused by fungi

While fungi do cause some diseases in animals, the diseases they cause in plants are far more numerous, and some of these may also have severe indirect effects on human health and well-being. At an introductory level, we shall explore examples of significant plant pathogens and examples of the different modes of attack employed by plant fungal pathogens, how plants defend against fungi and how fungal pathogens overcome the difficulty pose4 by having hosts that are largely static. 1. Dutch Elm Disease 2. Late Blight of Potato 3. Rusts 4. Powdery Mildews 5. Interactions between Plants & Pathogens 6. Investigating Plant Pathogens

1. Dutch Elm Disease Dutch elm disease first spread to Europe from the USA in the 1920s, and is caused by the ascomycete Ophiostoma ulmi.Lik most plant pathogens, its life cycle is complex; and particularly so in the case of Ophiostoma ulmi as itdepends on a vector for spread, the elm bark beetle.While the disease first came to prominence in the 1920s, the most severe outbreak has been since 1970, with over 20 million trees killed since that year in the UK. It is now accepted that this outbreak was caused by new, more agressive strains of the fungus which have been designated as a new species, Ophiostoma novo-ulmi. In brief, infection occurs when the fungus is carried into young twigs by the Elm bark beetle. The infection then spreads by mycelial growth and also through the host’s vascular system in the form of yeast. As the infection spreads, toxins (such as the protein cerato-ulmin) and fungal enzymes attack and digest the host tissue, and xylem vessels are blocked.

Vascular browning caused by Dutch Elm Disease © Gareth W. Griffith

Dutch elm disease is therefore an example of a vascular wilt disease.

As the infection proliferates, death of the tree will occur within a few months. The scent of a dying, tree attracts more bark beetles which breed in structures in the bark called breeding galleries. As the young beetles emerge from the galleries, they are contaminated with the spores of the fungus. Controlling Dutch elm disease has proved difficult. Breeding resistant varieties of trees takes decades. The other options are to spray with fungicide or insecticide (or both) to control the fungus or the vector. With trees the size of elms, this is particularly difficult to do with any measure of success. This leaves only the possibility of drastic action, the cutting down of infected trees, and this was not done early enough during the epidemic to be effective.

2. Late Blight Late blight of potatoes and related plants is caused by the Qomycete fungus Phytophthora infestans, a member of the Peronosporales. As discussed in the section on fungal taxonomy, Phytophthora is not a “real” fungus but rather member of the Kingdom Stramenophila. P. infestans was the first recognized plant pathogen; and to date ,it has caused the most serious epidemics of plant disease. The worst occurred in Ireland during the period 1845-1847. In an agriculturally based economy dependerit potatoes as the main food crop, the consequences were far reaching. The resulting potato famine led to the death of over a million people and forced emigration of a million others. P. infestans first reached Ireland via Europe, after infected potatoes were imported from Mexico, which is believed to be ancestral home of the pathogen. More recently, completely new populations of P. infestans have been detected in Britain, and in other European countries. These are thought to have been introduced to Europe following the drought of 1976, which led to the large-scale importation of potatoes. This r.mw population is genetically much more diverse than the old one, and since it includes a second mating type (only a single mating type having been present formerly in Britain) there is the potential for that diversity to increase still further, thereby allowing the pathogen to adapt more readily to agricultural control methods.

The new population of P. infestans already contains strains that are resistant to some of the front-line fungicides used to protect crops. In the USA, also, new strains have been detected, including the genotype designated US-8 which causes a highly aggressive, rapidly-spreading infection and is also resistant to the commonly-used phenylamide fungicides. phytophthora infestans does, however, have a number of ‘weaknesses’ in its life cycle. Infection occurs as a result of sporangia germinating on the moist leaf surfaces of potato plants. Zoospores are released and they infect the plant, germinating into hyphae which press into the plant. After 3-4 days, symptoms begin to appear on the plant, with necrotic lesions spreading from the point of infection. After a week, new sporangia are produced on the Ieaf surface, and these are released to infect new plants.

These sporangia represent the most delicate phase of the oomycete’s life cycle. If the air temperature drifts outside the range of 16-21o0, or the relative humidity drops below 75%, then spread is unlikely. If these conditions are maintained for more than 48 hours, then a Beaumont Period has occurred, and spread of the infection is highly likely. Weather monitoring allows farmers to anticipate the spread of blight, and spray potato crops at a point early enough to be effective. Detection of sporangia in air samples taken near crops may allow forecasting to be refined still further in the future.

© J Day

3_Rusts The pathogens mentioned earlier on this page are examples of necrotrophic pathogens (although Phytophthora infestans exhibits an initial biotrophic phase). Rusts, however (which belong to the Basidomycete subphylum Uredinomycetes), are completely biotrophic pathogens. They only parasitize their host plants, without killing them, though they do cause some tissue damage. Rust-infected plants may therefore appear quite healthy, apart from the ‘rusted’ appearance of the leaves due to the production of spores (usually orange or yellow).

A field bean plant infected with n Agriculture, University of Readinç University of Reading Image courtesy LTSN Biosciern ImageBank

Rusts are obligate biotrophs, meaning that they cannot survive without the presence of the host. The specificity of such fungi for their host is extremely high, and they will only infect one or a small number of host species. The small host range attacked by any given rust species means that it is essential for them not to kill off the host species, as happened with Phytophthora infestans in Ireland in the 1840s. But biotrophs such as rusts need to make loving as well, so they need to maximise their opportunity to drain nutrients from the host plant without killing it. As such, many rusts (and other biotrophs) have specialized structures called haustoria (singular, haustorium) which act to maximise contact with the host cells to allow good transfer of nutrients with excessively damaging the host’s tissues.

4. Powdery Mildews

Powdery mildews (Erysiphales), members of the phylum Ascomycota, are the most important pathogens of cereal crops in the UK, and cause significant reductions in yield when they strike — up to a 20 % loss as a result of the mildew continually drawing off the products of photosynthesis that would otherwise go into producing grain. Again, as with other biotrophs, the trend is for the development of a very narrow host range; an example of this is Erysiphe graminis var. tritici and Erysiphe graminis var. hordei, two varieties of the same species. The former will only infect wheat, whereas the latter will only infect barley!

Barley infected with powdery mildew © Gareth W. Griffith

Infection with powdery mildew occurs as conidia land on the leaf bf a Host plant. The conidia germinate to form a hypha called a germ tube. The end of the germ tube will form a swelling called an appressorium, tightly attached to the host surface. From the appressorium, a narrow hypha known as an infection peg is able to presses through the host plant’s epidermis. The mildew can then grow in the spaces between the plant cells and, like the rusts, it forms haustoria within the plant cells to siphon off nutrients from the plant lissues. To complete the disease cycle, hyphae appear on the surface, and conidia are released into the air, allowing the infection to be spread between plants.

5. Interactions between Plants and their Pathogens While most of us are familiar with the rudiments of the human immune system it is easy to forget that plants have evolved defences against their pathogens in fact, plants have been waging a full-scale arms race against their pathogens. In humans, the skin forms the first line of defence against infection. In plant this outer defence layer is the cuticle, a layer of waxy material above the epidermis. This stops many would-be plant pathogens from getting in on the act. However, there is a weak spot in the plant’s defence. In order to exchange carbon dioxide and oxygen for photosynthesis, plants have pores on their leaf surface called stomata (singular, stoma). These pores are ideal back-door entrances for fungal pathogens to get in (shown on the right).

Top view (point to activate). Side view (point activate).

Other fungi have an enzyme called cutinase which seems to cut up the cuticle so the fungi can get in — but this has proved difficult to prove!

So if our plant pathogen has got in, what can the plant do to stop it from getting any further?

Well, the next lines of defence are molecules called phytoanticipins These are ready-made and act in a general way against the fungi. If someone were to ask you for an example of a phytoanticipin, then saponin would be a good place to start. This is found in tomatoes, and is toxic to most fungal pathogens as it mixes with the fats in fungal cell membranes and causes the cells to leak, But fungi have a massive biochemical toolkit, and some fungi have developed an enzyme that can break down the saponin and as a result, they can grow the plants. The next part of the plant’s defences against fungi isn’t chemical, but rather structural. Plant cell walls are characterized by being rigid, and full of cellulose and other polysaccharides. When a plant is infected by a fungus that grows as hyphae the cell wall can thicken dramatically to form a papilla, which grows around the invading hyphae, preventing them from going any further. However the fungi have enzymes capable of breaking down the cellulose-based papillae, so plants often add lignin, the brown wood polymer. This is difficult for most fungi to break down, as many decomposer fungi know. Lignin is made of many phenolic compounds, similar to the type we use as antiseptics and these tend to saturate the area around the invading fungus, often killing it However, this is only a stop-gap action, to allow the, plants to get the next line of defence ready in time. The next step is to try to sacrifice the infected cells with a massive amount of oxidation. While we think of oxygen as being essential to life, on the molecular scale, oxygen atoms with extra unpaired electrons (called radicals) can do much to damage cells, particularly DNA. plants have the molecular machinery to take oxygen from the atmosphere and use an electron carrier which will give the oxygen a spare electron, making into highly reactive ion known as superoxide. Quickly, the superoxide is converted into hydrogen peroxide which, like phenolics, is used by humans as a disinfectant. Hydrogen peroxide can then react with the proteins of the plant cell wall to strengthen it: The production of hydrogen peroxide from superoxide is found in animals too as a response to infection or damage to tissue. Animals use hydrogen peroxide as a poison to kill invading bacteria. However, the toxic hydrogen peroxide often seeps into the surrounding tissue and causes inflammation and damage to the animals’ cells as well. Plants use this phenomenon to their advantage, and the cells involved in the. oxidative burst often die due to the toxic levels of hydrogen peroxide. This forces the fungus to try and grow through the highly toxic dead cells. Quite often, the fungus can’t. . The oxidative burst mentioned above often activates metabolic pathways. that produce molecules called phytoalexins. These molecules often act in similar way to antibiotics, by inhibiting fungal enzymes and blocking the synthesis of important molecules in the invading fungus. Some phytoalexins however activate some of the host’s own enzymes, such as chitinase, which breaks down the fungal cell wall. Some fungi have got ahead of the game, and can break down the phytoalexins the plants have used to try and break the fungi themselves down! The other side of the battle between plants and fungi is often quite complex. Vascular wilt pathogens such as Fusarium oxysporurn and Ophiostoma ulmi disrupt the plant’s delicate regulation of water by growing in the xylem vessels that carry water up the plant, causing the plant to dehydrate and die. Some fungi, like Ophiostoma ulmi, also use toxins to damage plants. But perhaps the most interesting way a fungal pathogen causes disease in plants is the. Foolish Seedling Disease caused by Giberella fungi. This disease involves increased growth in the plant, and destroyed 40% of Japans' rice crop in 1809. It was first isolated in 1908 by the Japanese pathologist Hori, and subsequent studies identified a growth promoting substance that they called a Giberellin. This is produced by the fungus, and causes the seedling to grow beyond their means and die. Other work then found giberellins produced by the plants themselves. Today, giberellins are mainly recognized as plant hormones that regulate growth, flowering, seed germination and so forth in a wide range of plants.

8