Fungal polygalacturonase activity reflects susceptibility of carnation cultivars to fusarium wilt

Abstract

Carnation cultivars with different levels of partial resistance were inoculated with race 2 of Fusarium oxysporum f.sp. dianthi and monitored for accumulation of host phytoalexins, fungal escape from compartmentalization, production of fungal pectin-degrading enzymes and development of external disease symptoms. Accumulation of phytoalexins, assessed after 10 days in the first 5 cm above the inoculation site, was weakly (methoxydianthramide S) or not (hydroxydianthalexin B) correlated with resistance levels after 12 weeks. Fungal escape from compartmentalization, assessed after 3 weeks as percentages colonized plants at 8 cm above the inoculation site, was highly correlated with expression of susceptibility after 12 weeks. Polygalacturonase (PG) activity, assessed after 4 weeks in the first 5 cm above the inoculation site, was highly correlated to final disease development. Linear increases in disease severity were accompanied by quadratic increases in PG activity. In contrast to water-treated plants, that lacked any PG activity, inoculated plants contained two main groups of fungal PGs, the dominant forms of which had estimated pI values of 7.0 and minimally 9.5, respectively. Compared to those of the first group, enzymes of the second group were produced only in trace amounts in liquid media containing pectin or polygalacturonate as sole source of carbon. On these media, the fungus also produced a pectin methyl esterase (PME) with an estimated pI of 9.3. Besides PMEs of host origin, inoculated plants of susceptible cultivars contained the fungal PME while no more than traces were found in resistant ones.Assessment of phytoalexin production by the host during defense responses cannot replace monitoring of external symptoms as a resistance test. Assessment of fungal growth, whether by reisolations above the compartmentalization area or by measurement of PG activity, provides a both rapid and reliable prediction of disease development.