(1,9). However, field observations indicated that the degree of clonal reaction to the toxin varied throughout the year. Initially, it was thought that either the pathogen cultures were losing their ability to produce toxin or that toxin solutions were losing their activity. Neither proved to be the case, so studies were initiated to determine possible host variability caused by environmental parameters. Since day length had no effect on susceptibility, studies involving the effect of temperature were initiated. This report documents the monthly deviation in clonal susceptibility and summarizes studies designed to better understand the influence temperature has on host-toxin interactions. Brief reports of this study (2, 11) have been published. Recently, the effects of temperature on the induction of resistance of pear leaves to Alteraria kikuchiana toxin has been reported (7).
Three mutants selected from a population of sugarcane clone H54-775 that had been irradiated with 3 kR gamma-radiation all lacked toxin-binding protein activity. This activity previously had been shown to be essential for eye spot disease susceptibility and was demonstrated in the susceptible parent clone H54-775. In one mutant, the biochemical, immunochemical, and electrophoretic mobilities of the toxin-binding protein were all modified.
Sugarcane rooting was inhibited by Ceratocystis paradoxa on both pathogen-invaded setts and disease-free setts suspended above cultures of the fungus. Root inhibition was not correlated with differences in clonal susceptibility. Volatiles from cultures of the pathogen caused root inhibition and a concomitant rise in host-tissue production of ethylene. Apparently the host tissue is stimulated to produce ethylene both directly by tissue invasion and indirectly by fungal volatiles. The ethylene produced is then in part responsible for the observed root inhibition.
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