The phytotoxicity of some phenolic metabolic products of Ophiostoma ulmi to ulmus sp.

Abstract

The Clo phenolic acids, 2,4-dihydroxy-6-acetonylbenzoic acid (1) and its 6-(l-hydroxyacetonyl) (2) and 6-pyruvyl (3) analogues, metabolic products of O, ulmi on a chemically defined medium are also produced on elm tissue medium but are rapidly metabolised once the carbon source is exhausted. The phytotoxicity to cut shoots of U. glabra and U. hollandica of these acids and their 4-0-methyl ethers (4-6 respectively) and of 4-hydroxyphenylacetic acid (7) has been investigated. None of the Clo acids consistently caused wilting or leaf necrosis in U. glabra but all three were toxic to U. hollandica. Diaporthic acid (4) caused severe leaf necrosis in both Ulmus sp. and the phenolic acid (7) caused wilting and necrosis of U. glabra shoots. Attempts to reproduce these effects in rooted U. glabra saplings were unsuccessful. Autoradiography of U. glabra shoots treated with [14C]-labelled acids (2) and (4) showed a uniform distribution of radioactivity in the tissues, but the labelled acids could not be recovered. There is no evidence that the low molecular weight metabolic products of O. ulmi are toxic to rooted saplings or proof that they are formed in vivo.

De novo biosynthesis of defense root exudates in response to Fusarium attack in barley

“…The detected 4‐hydroxyphenylacetic acid is known to be phytotoxic (Aoki et al. , 1963) and a product of some strains of the fungal pathogen Ophiostoma ulmi , as well as of several other plant pathogens (Claydon et al. , 1980).…”

“…We also detected an induction of benzoic and 4-hydroxyphenylacetic acids, which were probably secreted by Fusarium. The detected 4-hydroxyphenylacetic acid is known to be phytotoxic (Aoki et al, 1963) and a product of some strains of the fungal pathogen Ophiostoma ulmi, as well as of several other plant pathogens (Claydon et al, 1980). The constitutively detected benzoic acid could arise from both host and pathogen metabolism.…”

Characterization of the toxicity of cerato-ulmin, the toxin of Dutch elm disease

“…The PM30-R fraction, the PMIO-R fraction, and the UM2-F fraction caused no significant tox icity expressed as reduction in transpiration; wilt ing incidence was low for the PMIO-R fraction (after 24 h)and nil for the PM30-R fraction and the UM2-F fraction. The UM2-F fraction, which con tains low molecular weight components (<1 * 10 3 MW), might include phenolic carboxylic acids (metabolites also produced in vitro by C. ulmi) as reported by Claydon et al (1980). Pathogenicity of C. ulmi isolate X6.…”

“…C. Moreau, the pathogen of Dutch elm disease (DED), was initially demonstrated by Zentmyer (1942). Since then other researchers have isolated several metab olites from the culture filtrate of C. ulmi that have been claimed as toxins (Claydon et al 1980, Dimond et al 1949, Salemink et al 1965, Rebel 1969, Van Alfen & Turner 1975, Strobel et al 1978, Scheffer& Elgersma 1981, Nordin & Strobel 1981; however, none has been established as the toxin (pathotoxin) responsible for the development of DED.…”

The American elm and Dutch elm disease

“…Brasier and Gibbs (1976) have shown in crossing and subsequent inoculation experiments, that the F1 generation of the fungus does not exceed the virulence of its parents. Assumptions (based on circumstantial evidence) have been made that toxins, such as cerato ulmin (CU) (Takai 1980, Richards 1993, peptidorhamno-mannan (Claydon et al 1980, Nordin and Strobel 1981, Scheffer 1983, Scheffer et al 1987, glycopeptides and glycoprotein elicitors (Yang et al 1989) may function as factors of virulence. Binz and Canevascini (1996) stated that production of extra-cellular laccase may be important for the survival of the fungus in its host.…”