Normoergic NO-dependent changes, triggered by a SAR inducer in potato, create more potent defense responses to Phytophthora infestans

Abstract

In our experimental approach we examined how potato leaves exposed to a chemical agent might induce nitric oxide (NO) dependent biochemical modifications for future mobilization of an effective resistance to Phytophthora infestans. After potato leaf treatment with one of the following SAR inducers, i.e. β-aminobutyric acid (BABA), 2,6-dichloroisonicotinic acid (INA) or Laminarin, we observed enhanced NO generation concomitant with biochemical changes related to a slight superoxide anion (O2(-)) and hydrogen peroxide (H2O2) accumulation dependent on minimal NADPH oxidase and peroxidase activities, respectively. These rather normoergic changes, linked to the NO message, were mediated by the temporary down-regulation of S-nitrosoglutathione reductase (GSNOR). In turn, after challenge inoculation signal amplification promoted potato resistance manifested in the up-regulation of GSNOR activity tuned with the depletion of the SNO pool, which was observed by our team earlier (Floryszak-Wieczorek et al., 2012). Moreover, hyperergic defense responses related to an early and rapid O2(-)and H2O2 overproduction together with a temporary increase in NADPH oxidase and peroxidase activities were noted. BABA treatment was the most effective against P. infestans resulting in the enhanced activity of β-1,3-glucanase and callose deposition. Our results indicate that NO-mediated biochemical modifications might play an important role in creating more potent defense responses of potato to a subsequent P. infestans attack.

Keywords: 2,6-dichloroisonicotinic acid; BABA; Chemical agents; DAF-2DA; GSNO; GSNOR; H(2)O(2); INA; LAM; Laminarin; NO; Nitric oxide; O(2)(−); PR2; Phytophthora infestans; Potato; S-nitrosoglutathione; S-nitrosoglutathione reductase; S-nitrosothiols; SAR; SNO; Systemic acquired resistance; diaminofluoresceine diacetate; hydrogen peroxide; nitric oxide; superoxide anion; systemic acquired resistance; β-1,3-glucanase; β-aminobutyric acid.