Read Aloud the Text Content

This audio was created by Woord's Text to Speech service by content creators from all around the world.

Text Content or SSML code:

3.1 Life cycle and disease development in C. purpurea The major aspects of the life cycle of C. purpurea are presented in Fig. 5. Primary infection by C. purpurea is initiated by ascospores ejected from perithecia, which are formed in spring from germinating overwintering structures, the sclerotia. The fungus can infect a broad range of grasses or cereals, but is highly organ specific, as it infects only the ovaries. The mechanism underlying this specificity is unclear, but may be mediated by interaction with the surface of the stigmatic hairs where the spores germinate at anthesis.The germ tubes penetrate the plant cuticle (there is no evidence for the involvement of physical pressure and no specific infection structures are formed). After penetration, the fungus follows the path of the pollen tube, growing in thick hyphal bundles almost without any branching. Only at the base of the ovary do the hyphae leave the pollen tube path and tap the vascular tissue; only then is a ‘normal’ branched mycelium formed (the so-called sphacelium), which colonizes the whole ovary and produces conidia, which are secreted (about 7 days post infection, dpi), together with plant phloem exudates, as honeydew and initiate a secondary infection by drop inoculation or transfer by insects. About 2 weeks post-infection, the production of honeydew ceases and the development of sclerotia is initiated; they serve as overwintering structures and exclusively (at least in pathogenic field isolates) contain the ergot alkaloids. This infection cycle has the following specific aspects that make C. purpurea an interesting model system for plant pathologists and cell biologists alike. 1. Strict organ specificity, the molecular basis of which is not yet understood. 2. Lack of detectable plant defence reactions; this is probably a result of mimicry of pollen tube growth, although molecular analyses suggest that the fungus is recognized but that defence reactions are repressed (see below). 3. Strict polar, oriented, almost unbranched growth in the first infection stage, recapitulating, for example, the oriented growth of axons; the cues/signals guiding this oriented growth are still unknown. 4. Biotrophic life style: the fungus shows no necrotrophic growth symptoms (necroses, rapid host cell death) in any phase of infection; it grows mostly intercellularly, but intracellular hyphae have also been described which could have haustoria-like function. However, C. purpurea can be easily grown in culture; it is an ecologically obligate pathogen obtaining nutrients in planta exclusively from living tissue and maintaining host cell viability for extended periods. These interesting features have stimulated a detailed molecular analysis of this system in recent years (see below). 3.2 Economic impact of ergot today Today, several methods have been developed to reduce the risk of ergot infection in most cereal crops with the consequence that ergotism as a human disease has almost been eliminated. These methods include changes in crop rotation, deeper ploughing and sifting out of the sclerotia (Mielke, 1993). In addition, the application of fungicides, breeding for disease resistance and crossing of natural rye with hybrid rye reduce the infection of rye with C. purpurea (summarized in Mielke, 2000). In the European Union, the amount of ergot in grain used for human food is restricted to 0.05% at a maximum. This corresponds to an average of 1 mg alkaloids per kilogram based on an average alkaloid content of about 0.2% (Appelt and Ellner, 2008). For animal feed, 0.1% grain samples containing 0.1% of sclerotia or pieces thereof can be tolerated. Similar standards are applied in the USA and Canada (Mirdita et al., 2008). Selling grain exceeding these thresholds leads to financial suffering. According to Betz et al. (1998) incurred costs of seed cleaning amount to more than 2€/dt of grain. After cleaning of the grain, the costly disposal of ergot as hazardous waste increases the economical losses evoked by ergot infestation (Münzing, 1999). In Germany, as a result of changes in cultivation and crop rotation, ergot did not cause any severe problems in rye cultivation until the 1980s. However, at the beginning of the 1990s, increased occurrence of infection in the cultivation of hybrid rye with C. purpurea was observed (Mielke, 2000). The increasing cultivation of hybrid rye itself seems to have contributed to the increased occurrence of ergot infestation since the 1980s (Mielke, 1993). Another reason might be the increasing cultivation of triticale (cited in Mielke, 2000); in addition, the grass borders around the field perimeters may contribute to the infection of rye as they can serve as alternative hosts for C. purpurea. Underlining the average infection data for C. purpurea, annual investigations of the Federal Research Institute of Nutrition and Food (Max Rubner Institute) between 1995 and 2004 revealed a relatively constant level of ergot contamination in the analysed rye samples of about 0.11% w/w. Nevertheless, depending on different climatic and weather conditions, as well as differences in the employed cultivars, the contamination of rye with ergot differs considerably (Lindhauer et al., 2005). In 1998, massive infestation of rye in some parts of Germany led to almost a total loss of the harvest (Mielke, 2000). In addition, in the US Midwest in 2005, widespread occurrence of ergot in barley was reported (Schwarz et al., 2006). In addition, ergot causes problems by poisoning grazing animals as a result of the consumption of ergot alkaloids. Ergot alkaloids ingested by livestock may be ultimately derived from two different sources. Ergot alkaloids produced by Claviceps spp. on ears of pasture grasses and feed grain crops that are ingested by livestock (Blaney et al., 2000) are particularly problematic if the animals are allowed to graze on grass that is flowering (Cross, 2003). However, ergot alkaloids are also produced by endophytic fungi of the genera Epichloë, Neotyphodium and Balansia belonging to the family Clavicipitaceae (Schardl et al., 2009; Zhang et al., 2006). These fungi are symbionts of many grasses of the subfamily Pooideae and colonize the intercellular spaces of all the above-ground parts of the plant, including the reproductive tissues, but do not infect the root (Schardl, 1996). The sexual endophytes are classified as Epichloë and Balansia species, whereas their asexual counterparts are termed Neotyphodium and Ephelis species, respectively. The endophytes form systemic infections and derive nutrients fromthe extracellular substrates of the hosts.Many, but not all, of these fungi produce ergot alkaloids when associated with their host plant. They are important agents of biological plant protection against insects and grazing vertebrates (Bush et al., 1997; Schardl and Phillips, 1997). In addition, it has been shown for tall fescue infected with Neotyphodium coenophialum and for perennial ryegrass infected with Neotyphodium lolii symbioses that the grasses exhibit enhanced competitiveness, improved root growth and increased drought and mineral stress tolerance (Arechavaleta et al., 1989; Malinowski and Belesky, 2000; Popay and Bonos, 2005). In addition to these benefits for endophyte infected grasses, deleterious effects on livestock may occur. Toxicosis problems suffered by animals grazing on tall fescue were first noted in the 1930s, and in 1990 the estimated economic loss for the beef cattle industry in the USA was more than $600 million (Hoveland, 1993).Affected livestock show loss of appetite and reduced weight gain, fat necrosis, loss of body temperature control (hyperthermia), convulsions, rough hair coats and reduced fertility, and lactating cows show reduced milk production (Porter and Thompson, 1992; Schmid and Osborne, 1993; Thomson and Stuedemann, 1993). Affected animals, particularly horses, can also suffer increased frequencies of still-births, where foals are characteristically delivered several weeks after normal gestation and show distortions in bone structure (Cross et al., 1995). Another symptom is fescue foot, usually seen in the winter months, where affected animals suffer from dry gangrene of the extremities. The effects of ergot alkaloid poisoning are mainly attributed to the ergopeptine ergovaline; however, transport across ruminant gastric membranes is much higher for intermediate lysergyl compounds than for ergopeptines, suggesting that intermediate ergot alkaloids may also play a significant role (Hill et al., 2001). During the past decades, ergot of sorghum has emerged to become a worldwide threat to the sorghum industry, and has gained great economical importance because of its rapid spread throughout the world. Sorghum (Sorghum bicolor) is the world’s fifth most important cereal crop, which is grown on 45 million hectares and is used for food, livestock feeding, beverage production and industrial purposes. Ergot of sorghum affects nonfertilized ovaries in sorghum male -sterile plants and infects hybrids if there is pollen sterility at flowering time.