Defense response mechanisms of Pinus koraiensis against Bursaphelenchus xylophilus.

Abstract

Bursaphelenchus xylophilus (Steiner & Buhrer) Nickle is a widely distributed quarantine nematode that causes pine wilt disease, posing serious threats to pine forests worldwide. Nevertheless, the mechanism underlying pine resistance remains ambiguous. Research was conducted to reveal the physiological and molecular mechanisms involved in Pinus koraiensis resistance to B. xylophilus infection. The changes in reactive oxidative species, stress hormones, osmotic regulators, antioxidant enzymes, antioxidants, and transcriptomes were monitored. The results showed that after being inoculated with B. xylophilus for 30 days, some needles of P. koraiensis showed external symptoms of chlorosis, wilting, and drooping. B. xylophilus induced a higher level of signal transduction molecules overall, such as hydrogen peroxide (H2O2), superoxide anion radical (O2-), salicylic acid (SA), and jasmonic acid (JA). Besides, B. xylophilus caused a reduction in superoxide dismutase (SOD) and catalase (CAT) activities from 3 days after inoculation but increased peroxidase (POD) activity at 1, 3, and 30 days after inoculation. Following B. xylophilus infection, we also observed coordinated metabolic changes: significant reduction in soluble sugar (SS) and total phenolic contrasting with pronounced accumulation of proline (Pro) and flavonoids. Furthermore, the results of transcriptome analysis showed that the metabolic pathways in which differentially expressed genes were mainly enriched included flavonoid biosynthesis, phenylpropanoid biosynthesis, plant hormone signal transduction, and plant-pathogen interaction. Our findings demonstrated that the metabolic pathways of signaling transduction and secondary metabolite biosynthesis, as well as several disease resistance-related genes and substances of P. koraiensis, are induced by B. xylophilus infection, and they collectively contribute to the defense response against nematode infestation. These findings will provide a theoretical basis for the further exploration of the defense mechanisms of host pines against pine wilt disease.