Sclerotinia Infection Model
Plant Infection by S. sclerotiorum
Carpogenic germination of sclerotia is stimulated by periods of continuous soil moisture. Apothecia are formed on the soil surface from which ascospores are released into the air. Infection of most crop species is principally associated with ascospores but direct infection of healthy, intact plant tissue from germinating ascospores usually does not occur. Instead, infection of leaf and stem tissue of healthy plants results only when germinating ascospores colonize dead or senescing tissues, usually flower parts such as abscised petals, prior to the formation of infection structures and penetration. Myceliogenic germination of sclerotia at the soil surface can also result in colonization of dead organic matter with subsequent infection of adjacent living plants. However, in some crops, for example sunflower myceliogenic germination of sclerotia can directly initiate the infection process of the roots and basal stem resulting in wilt. The stimulus for myceliogenic germination and infection in sunflower is not known but likely depends on nutritional signals in the rhizosphere derived from host plants.
The infection process
Infection of healthy tissue depends on the formation of an appressorium, which may be simple or complex in structure depending on the host surface. In most cases, penetration is directly through the cuticle and not through stomata. Appressoria develop from terminal dichotomous branching of hyphae growing on the host surface and consist of a pad of broad, multi-septate, short hyphae that are orientated perpendicular to the host surface to which they are attached by mucilage. Complex appressoria are often referred to as infection cushions. Although earlier workers considered penetration of the cuticle to be a purely mechanical process there is strong evidence from ultra-structural studies that enzymatic digestion of the cuticle also plays a role in the penetration process. Little is known about S. sclerotiorum cutinases, however, the genome encodes at least four cutinase-like enzymes (Hegedus unpublished). A large vesicle, formed at the appressorium tip prior to penetration, appears to be released into the host cuticle during penetration. After penetration of the cuticle, a subcuticular vesicle forms from which large hyphae fan out growing over and dissolving the subcuticular wall of the epidermis.
Infection by enzymatic degratation of the epidemic cells: Oxalic acid works in concern with cell wall degrading enzymes, such as polygalacturonase (PG), to bring about the destruction of host tissue by creating an environment conducive for PG attack on pectin in the middle lamella. This in turn releases low molecular weight derivatives that induce the expression of additional PG genes. Indeed, overall PG activity is induced by pectin or pectin-derived monosaccharides, such as galacturonic acid, and is repressed by the presence of glucose. Examination of the expression patterns of individual Sspg genes has revealed that the interplay among PGs and with the host during the various stages of infection is finely co-ordinated. (Dwayne D. Hegedus *, S. Roger Rimmer: Sclerotinia sclerotiorum: When ‘‘to be or not to be’’ a pathogen? FEMS Microbiology Letters 251 (2005) 177–184)
Looking for Climate Conditions for Infection of S. sclerotiorum has to take consideration of the apothecia formation, the sporulation, the direct infection by apothecia (even if it does not take place very frequent) and the infection from established mycelia by encymatic degradation of the epidemic cells .
Apothecia formation and sporulation takes place if a rain of more than 8 mm is followed by a period of high relative humdiity lasting longer than 20 hours at optimum temperature of 21°C to 26°C.
Direct Infection by Apothecia can be expected after a leaf wetness period followed by 16 hours of relative humdity higher than 90% under optimum 21°C to 26°C ("appressoria infection"). Wheras saprophytic growth followed by encymatic degratation of the epidermic cells ("hydrolytic infection") can be expected under a slightly lower relative humditiy of 80% lasting for a period of 24 hours under optimum conditions of 21°C to 26°C.
1 Lumsden, R.D. (1976) Pectolytic enzymes of Sclerotinia sclerotiorum and their localization on infected bean. Can. J. Bot. 54,2630–2641.
2 Tariq, V.N. and Jeffries, P. (1984) Appressorium formation by Sclerotinia sclerotiorum: scanning electron microscopy. Trans. Brit. Mycol. Soc. 82, 645–651.
3 Boyle, C. (1921) Studies in the physiology of parasitism. VI. Infection by Sclerotinia libertiana. Ann. Bot. 35, 337–347.
4 Abawi, G.S., Polach, F.J. and Molin, W.T. (1975) Infection of bean by ascospores of Whetzelinia sclerotiorum. Phytopathology 65, 673–678.
5 Tariq, V.N. and Jeffries, P. (1986) Ultrastructure of penetration of Phaseolus spp. by Sclerotinia sclerotiorum. Can. J. Bot. 64, 2909– 2915.
6 Marciano, P., Di Lenna, P. and Magro, P. (1983) Oxalic acid, cell wall degrading enzymes and pH in pathogenesis and their significance in the virulence of two Sclerotinia sclerotiorum isolates on sunflower. Physiol. Plant Pathol. 22, 339–345.
7 Fraissinet-Tachet, L. and Fevre, M. (1996) Regulation by galacturonic acid of ppectinolytic enzyme production by Sclerotinia sclerotiorum. Curr. Microbiol. 33, 49–53.