We conducted dose-response studies of the toxicity of salicylate (SA; a putative signal molecule for enhancement of plant disease resistance [EPDR]) toward plant-pathogenic fungi. SA concentrations >10.0 mM were required for complete inhibition of fungal growth from mycelial plugs. SA doses of 2.0-5.0 mM typically reduced fungal growth by 50%, whereas doses of 0.5 mM or lower had little or no effect on fungal growth. However, growth of several test fungi was completely inhibited by 2.0 mM SA combined with concentrations of cupric chloride, antifungal bacterial culture fluids, or neem extract that were otherwise only slightly to moderately inhibitory. We conclude that (1) endogenous SA concentrations (up to 10.0-100.0 [jlM) are unlikely to directly inhibit fungi in plants, (2) concentrations of exogenous SA applied for EPDR (2.0-10.0 mM) are likely to be only moderately inhibitory to fungi, and (3) additions of other antifungal materials with which SA synergizes may enhance the antifungal activity of SA applied to plant surfaces for EPDR. The latter conclusion provides a rationale for further study of the synergistic interactions of moderately active antifungal materials for practical plant disease control.
New rudimentary (r) mutants have been isolated following mutagenesis with ethyl methanesulfonate (rLE), ICR-170 (rLI) and X rays (rLX) . From wing phenotype measurements on hamoallelic females, it has been shown that the rLE mutant series includes several leaky alleles, as well as alleles that produce moderate and strong r phenotypes. All of the tested rLI alleles yielded strong r phenotypes in homoallelic females, whereas the rLX series was found to include both moderate and strong alleles. Based on allele complementation for the wing phenotype, it was found that all three mutant series include both complementing and noncomplementing alleles, but the relative frequencies of these two types of alleles differ considerably among the three series. Complementing alleles comprise most of the rLE mutant series (19 of 25) and almost one-half of the rLX series (five of 12), while only one of 16 rLI mutants is a complementing allele. Data from enzyme assays of mutants mostly support the direct correlation of genetic complementation units with the activities of the first three enzymes in the de novo pyrimidine biosynthetic pathway. All of these findings are discussed in light of evidence that these three enzymes are contained within a tri-enzyme complex in animals. We conclude that the available genetic evidence supports the contention that the trienzyme complex is encoded by a single mRNA.
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