Induction of pathogen resistance and pathogenesis‐related genes in tobacco by a heat‐stable Trichoderma mycelial extract and plant signal messengers

Abstract

Heat‐stable mycelial extracts of the nonpathogenic fungus Trichoderma longibrachiatum induced resistance in tobacco seedlings (Nicotiana tabacum L. cv. Wisconsin 38) to the pathogen Phytophthora parasitica var. nicotianae (race 0), which did not involve a hypersensitive response. Resistance could not be induced with mycelial extract prepared in the same manner from P. parasitica. The nonpathogenic mycelial extract induced expression of PR‐1b and osmotin (PR‐5) genes to a higher level than did mycelial extract from the pathogenic fungus. The tissue‐specific pattern of PR gene induction by the nonpathogenic mycelial extract was different from that of the pathogenic mycelial extract and was consistent with the ability of the former to cause disease resistance. The expression patterns of these two PR genes and the accumulations of their encoded proteins also were affected by salicylic acid (SA), methyl jasmonate (MeJA), ethylene (E) and combinations of these plant signal messengers. However, only combined SA and MeJA treatment mimicked the pattern of PR gene mRNA and protein accumulation induced by the nonpathogenic mycelial extract. E inhibitors blocked both mycelial extract‐induced and SA/MeJA‐induced PR gene expression, and the cis pattern of responsiveness on the osmotin promoter was the same for the mycelial extract, SA, E, or E/MeJA. Seedlings treated with P. parasitica spores in the presence of SA/MeJA were protected from pathogen colonization. However, these seedlings exhibited symptoms of cell death (disease symptoms) both in the absence and presence of P. parasitica spores, in contrast to seedlings treated with nonpathogenic mycelial extract, which remained healthy. These results suggest that the signal transduction pathways for elicitation of defense responses by exogenously applied heat‐stable nonpathogenic mycelial extract and SA/MeJA overlap at the point of PR protein induction but are not identical.

Identification of a locus controlling Verticillium disease symptom response in Arabidopsis thaliana

“…Cev1 mutant plants also have short roots with an excess of root hairs and increased anthocyanin accumulation in petioles (Ellis and Turner, 2001), whereas crp5 plants present an altered trichome development and an early senescence phenotype (Bowling et al ., 1997; Yoshida et al ., 2002). This complexity is further evidenced by the observation that altering the levels of host signal molecules may mimic but not exactly duplicate pathogen‐induced symptoms (Bent et al ., 1992; Chang et al ., 1997). The dependence of interactions of pathogen with host signaling on the host genetic status is emphasized by the distinct difference in flowering response by Columbia and C‐24 whereby V. dahliae accelerates flowering in Columbia and delays flowering in C‐24 (Figure 1c).…”

Trichoderma- from lab bench to field application: Looking back over 50 years

“…Indirect evidence of plant ISR by Trichoderma was first described by (Calderon et al, 1993) through induction of hypersensitive response (HR) and phytoalexin synthesis by T. viride cellulase in grapevine cell cultures. Later, Chang et al (1997) demonstrated the capability of heat-stable mycelial extracts of T. longibrachiatum to induce disease resistance against Phytophthora parasitica by induction of higher level of PR-1b and PR-5 in tobacco, Nicotiana tabacum (Chang et al, 1997). In addition, reports on soil inoculation with T. harzianumT39 imparted resistance to leaves of bean plants, that is, parts spatially separated from the site of inoculation against B. cinerea and C. lindemuthianum have also been documented (Bigirimana et al, 1997;De Meyer et al, 1998).…”

Microbial Induction of Resistance to Pathogens

“…Thus, cellulose from Trichoderma viride was found to induce plant defence responses in grapevine cell cultures (Calderón et al, 1993), while control of Phytophthora parasitica var. nicotianae on tobacco by T. longibrachiatum was linked to the induction of plant defences (Chang et al, 1997). Subsequent work on control of B. cinerea on a number of plant species using the BCA T. harzianum T39 provided further evidence for the involvement of induced plant defences (De Meyer et al, 1998).…”