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The disease is caused by three different Claviceps species, namely C. africana, C. sorghi and C. sorghicola. In 1917, sorghum ergot caused by C. sorghi was first described in India (McRae, 1917; cited in Pažoutová et al., 2000) and, thereafter, in 1923 in Kenya (Bandyopadhyay et al., 1998), where it was identified as C. africana (Frederickson et al., 1991). The disease did not account for considerable economical losses until the introduction of male-sterile sorghum in the 1960s (Bandyopadhyay et al., 1998; Pažoutová and Frederickson, 2005), which is highly susceptible to infection with Claviceps spp. Consequently, together with the development and expansion of F1 hybrid seed production, ergot spread across Africa and Asia (reviewed in Bandyopadhyay et al., 1998; Pažoutová et al., 2000). Economic losses are caused by a reduction in seed quality and a reduced yield, creation of difficulties in harvesting and threshing, and problems in the international trade of contaminated seed. In addition, as outlined above, alkaloid-containing sclerotia carry the risk of intoxication of livestock when being fed with ergot-contaminated sorghum (Blaney et al., 2000). As a consequence, the limit for sclerotia/sphacelia in grains for stockfeed has been reduced to 0.1% w/w in Australia (Chakraborty and Ryley, 2008). Over the past decades, ergot of sorghum has become a global threat. Losses of up to 80% in India and 25% in Zimbabwe have been reported (Bandyopadhyay et al., 1998). Probably because of its ability to produce airborne secondary conidia, it is C. africana that has emerged as the dominant causal agent of ergot sorghum worldwide, almost completely replacing C. sorghi in India (Pažoutová et al., 2000). In 1995, the first occurrence of sorghum ergot caused by C. africana outside Africa and Asia was reported in Brazil, where it caused a rapid and widespread epidemic. Subsequently, the disease has rapidly distributed to South, Central and North America and the Caribbean (summarized, for example, in Bandyopadhyay et al., 1998). The ability of C. africana to produce (asexual) airborne secondary conidia (Frederickson et al., 1993) that travel moderate distances is thought to be one of the reasons for its rapid international dispersal. In 1997, ergot of sorghum caused widespread economic loss in the Texas Panhandle (Prom et al., 2005), where 95% of the hybrid sorghum seed supply of the USA is produced. In 2002, sorghum ergot affected 87% and, in 2004, 90% of the seed production fields in the Panhandle (Workneh et al., 2006). Hybrid seed is especially affected as the disease raises difficulties not only in the production of hybrid seed, but also with seed distribution, as the seed obtained is restricted. After its introduction into the Americas in 1995, C. africana was reported in Queensland, Australia in 1996 (Ryley et al., 1996) and, within a month, the disease had spread over an area of approximately 70 000 km2 (Bandyopadhyay et al., 1998). Today, the disease causes between 30% and 100% losses in nurseries and parent seed production (Chakraborty and Ryley, 2008). The origin of ergot introduction into Australia was probably India or another South Asian country. However, the means by which C. africana spread to Brazil in 1995 and to Australia in 1996 still remains to be elucidated (Bandyopadhyay et al., 1998; Chakraborty and Ryley, 2008; Pažoutová and Frederickson, 2005). Nevertheless, it seems to be beyond any doubt that climatic conditions, such as low temperatures and humid weather before and during flowering, contribute to ergot outbreaks and the rapid distribution of the disease (see, for example, Bandyopadhyay et al., 1998; Ryley and Chakraborty, 2008;Workneh and Rush, 2006). 4. MOLECULAR ASPECTS OF HOST–PATHOGEN INTERACTION Claviceps purpurea is regarded as a plant pathogen, as reproduction of the infected ear is altered. However, protection from grazing animals may balance this reproductive cost, implying that a beneficial ‘partnership’ of host and pathogen has evolved. A complex network of growth and developmental regulation to overcome plant defence mechanisms must underlie the unique infection pattern. Some of the strategies invented by the fungus to accomplish biotrophic growth in its model host Secale cereale (rye) are discussed here. An invaluable tool in analysing in detail the function of genes and in identifying virulence/pathogenicity factors is a knock-out approach. In Table 2, the knock-out mutants currently available are described. Phytopathogenic fungi have generated different mechanisms to overcome the first defence barrier, the plant cell wall. One is the formation of specialized penetration structures applying great force, called appressoria. Penetration structures have never been observed in C. purpurea, suggesting that penetration must be achieved by loosening of the cell wall by enzyme secretion. Grasses have developed a special cell wall type containing mainly glucuronoarabinoxylans, cellulose and b-1,3-glucan, and only small amounts of pectin. The detection of xylanase and b-1,3-glucanase (Giesbert et al., 1998; Tenberge, 1999) activity in planta indicates a role for cell wall degrading enzymes (CWDEs) in fungal host colonization. Cellulolytic activity, however, has been studied extensively, but could not be correlated with penetration (Müller et al., 1997). After penetration of the outer wall, the fungus grows mainly intercellularly, deriving nutrients from the degradation products of the pectic material present in the middle lamella (Tenberge et al., 1996). Double deletion of two putative endo-polygalacturonase genes showed drastic effects on pathogenicity, although colonization of the ovaries was not completely abolished, indicating that other enzymes compensate for the loss of galacturonase activity (Oeser et al., 2002). In biology,fungal hyphae,axons,pollentubes androot hairs are the most prominent examples of apical growth (Harris, 2006; Palanivelu and Preuss, 2000). Claviceps purpurea grows in the transmitting tissue, mimicking pollen tube growth, until the ovary base is reached and the pollen tube path is abandoned. The growth direction must be highly regulated at this stage of colonization as the fungus grows mainly without branching. After reaching the nutrient-rich phloem exudate, the fungus becomes highly branched and colonizes the entire ovary. The signals guiding and restricting fungal growth in the earliest infection stage are unknown. One hypothesis is based on the observation that the fungus follows and feeds on a pectin-rich trace in the transmitting tissue (Tenberge et al., 1996). During pectin degradation, calcium ions are released, putatively functioning as a guidance cue and possibly as a branching inhibitor. It has long been known that a tip high calcium gradient is necessary for polar growth (Jackson and Heath, 1993; Silverman-Gavrila and Lew, 2000). To elucidate whether high calcium levels in the surrounding medium are sensed by C. purpurea, functional analysis of a stretch-activated calcium channel (Mid1) was undertaken. Loss of mid1 leads to non-pathogenicity and increased sensitivity to cell wall stress, indicating that either ion sensing or cell wall composition are important for host colonization. An overall reduction in growth rate was suppressed on medium containing higher percentages of agar, indicating that cell wall defects of the mutant may impair force generation (J. Bormann, WWU Muenster, unpublished data). In this regard, it is interesting that deletion of the gene cpcot1, encoding an NDR-like kinase (Cpcot1), not only evoked hyperbranching, decreased growth rate and a penetration defect, but the wild-type phenotype was partial restored when grown under an overlay of 8% agar (Scheffer et al., 2005a). It is still unclear whether imposed pressure on hyphae during intercellularin planta growth plays a generalrole in growth regulation. Claviceps purpurea mutants that show altered morphology and/or altered cell wall structure are often found to be impaired in host colonization. For instance, a mutant lacking the mitogenactivated protein kinase (MAPK) Cpmk2 (homologue to yeast Slt2) is more sensitive to lysing enzyme, shows hyperbranched and coiled hyphae and reduced virulence; reduced virulence was also shown for Dcpmk1 (lacking a homologue of yeast Fus3/Kss1) (Mey et al., 2002a, b). Activation of MAPK depends on a two component sensor histidine kinase system. A class X histidine kinase has an influence on pathogenicity, stress tolerance and spore germination in C. purpurea (Nathues et al., 2007). These examples indicate that either cell wall stability is important to generate pressure during in planta growth or that altered gene regulation in these mutants may elicit a host response. Known elicitors of host defence include cell wall components, extracellular enzymes produced by the pathogen, and secreted small molecules, such as reactive oxygen species (ROS). However, ROS are known to act in the earliest defence reactions of plants. A first-hand role of these molecules is reinforcement of the host cell wall by cross-linking of cell wall proteins. Also triggered by ROS is the hypersensitive response (HR), a plant defence programme causing rapid necrosis at the proximate infection site, and induction of late defence genes in the surrounding tissue (Baker and Orlandi, 1995). As no HR was observed during C. purpurea infection of rye, the fungus might have evolved a strong antioxidant machinery to detoxify plant ROS.