Factors affecting infection cushion development by Rhizoctonia solani AG‐1 IA and IB on soybean leaves

Abstract

Infection cushions were formed by isolates of Rhizoctonia solani, anastomosis group 1 IA (AG-I I A, aerial blight) and AG-1 IB (web blight) on leaves ofall 10 soybean cullivars tested. Isolates of AG-1 IA and IB did not form infection cushions on soybean leaf surface replicas of either resistant or susceptible cultivars. More infection cushions were formed by isolates of AG-1 IA and IB on collodion membranes placed over leaves of susceptible cultivars compared with resistant cultivars. Isolates of AG-1 IC. AG-4 and AG-5, also formed infection cushions on soybean leaves. However, the isolates of other anastomosis groups did not form infection cushions on soybean leaves. Differential induction of infection cushion formation by the leaves of various plant species was observed, AG-1 IA formed infection cushions on more graminaceous hosts than AG-1 IB, Our results suggest that a chemical stimulus is needed for infection cushion formation. Glucose and 3-O-methylglucose repressed disease severity caused by AG-1 IA and IB isolates to the same extent. Disease severity and the number of infection c^shions formed on leaves of ten soybean cultivars were correlated. Fewer infection cushions were formed on resistant cultivars than on susceptible cultivars.

A nonpathogenic species of binucleateRhizoctoniainhibits the formation of infection structures caused byRhizoctonia solanion cucumber

“…This further proves the high correlation between the Marshall & Rush 1980b). The previous result was in accordance with Marshall and Rush (1980a), who found several factors affecting infection cushions development by R. solani on host tissues (Kousik et al 1994). This could be thigmodifferentiation, which is contact stimulus (Khadge et al 1963;Cubeta & Echandi 1991), or chemodifferentiation or response to chemical stimuli such as host exudates (Wyllie 1962;De Silva and Wood 1964;Van Etten et al 1967;Dodman et al 1968a;Marcus et al 1986).…”

“…R. solani AG4 penetrates cucumber seedlings by infection pegs from the basal part of an infection cushion (Flentje et al 1963) or directly through the hypocotyls surface with hyphal tips (Fukutomi & Takada 1979). In other crop plants, R. solani (AG4) infects through infection cushion and penetration stages (Dodman & Flentje 1970;Kousik et al 1994). In damping-off disease of cucumber, R. solani AG4 forms infection cushion and/or lobate appresoria on the hypocotyl surface (Fukutomi & Takada 1979;Villajuan-Abgona et al 1994).…”

Gene expression profiling of the plant pathogenic basidiomycetous fungus Rhizoctonia solani AG 4 reveals putative virulence factors

“…In this context, we discovered four pathogenesis-related genes in the W2 EST library (mimicking virulent conditions) and 17 pathogenesis-related genes in the W3 EST library (mimicking hypovirulent conditions) (TABLE III). Identification of more pathogenesisrelated genes in W3 EST library seemingly contradicts Kousik (1994) and Weinhold and Bowman (1974) and our observation that MeG-amended R. solani inoculum is less virulent than R. solani inoculum grown in medium without MeG. However, the discovery of a number of expressed pathogenesisrelated proteins in the hypovirulent EST library is not surprising when considering that MeG affects only one aspect of the infection process (González García et al 2006, Weinhold andBowman 1974).…”

“…To maximize the number of unique ESTs, the two libraries were from R. solani isolate Rs23A grown under different nitrogen and carbon source conditions to mimic virulent or hypovirulent conditions (Kousik et al 1994, Weinhold and Bowman 1974, Weinhold et al 1969). In addition, the two EST libraries were normalized to increase the probability of detecting rare species of mRNA.…”

In vitro analysis of host plant specificity in Rhizoctonia solani

“…As for rust fungi (Hoch & Staples, 1991), initiation of the infection process as a result of thigmo-differentiation has been suggested (De Silva & Wood, 1964;. However, most observations (Flentje et al, 1963;Marshal & Rush, 1980;Kousik et al, 1994;Keijer, 1996) support the hypothesis, originally put forward by Flentje (1957), that a chemical component is the principal determinant in the induction of infection cushions. Neither the nature of components involved nor the regulatory mechanism is known.…”