Abstract

Fusarium circinatum, the causal agent of pitch canker in pines and a cryptic endophyte of grasses, was examined for heritable variation in tolerance of the grass defense compound 2-benzoxazolinone (BOA). A diverse population of F. circinatum progeny was assayed for growth rate on potato dextrose agar amended with BOA. Matings were conducted to allow for selection of progeny with lower and higher tolerance of BOA. The results confirmed heritable variation in BOA tolerance in F. circinatum. A subset of differentially tolerant progeny was used for inoculations of growth chamber-grown Zea mays and greenhouse-grown Pinus radiata. No differences were detected in the rate of infection or extent of colonization of Z. mays inoculated with F. circinatum progeny differing in tolerance of BOA. Pitch canker symptoms in inoculated P. radiata trees showed that high BOA-tolerating isolates induced significantly longer lesion lengths than those induced by low BOA-tolerating isolates. Results from this study were consistent with the proposition that F. circinatum evolved from grass-colonizing ancestors and that pathogenicity to pine is a relatively recent evolutionary innovation.

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