The pinewood nematode (PWN) Bursaphelenchus xylophilus causes pine wilt disease, which results in substantial economic and environmental losses across pine forests worldwide. Although systemic acquired resistance (SAR) is effective in controlling PWN, the detailed mechanisms underlying the resistance to PWN are unclear. Here, we treated pine samples with two SAR elicitors, acibenzolar-S-methyl (ASM) and methyl salicylic acid (MeSA) and constructed an in vivo transcriptome of PWN-infected pines under SAR conditions. A total of 252 million clean reads were obtained and mapped onto the reference genome. Compared with untreated pines, 1091 and 1139 genes were differentially upregulated following the ASM and MeSA treatments, respectively. Among these, 650 genes showed co-expression patterns in response to both SAR elicitors. Analysis of these patterns indicated a functional linkage among photorespiration, peroxisome, and glycine metabolism, which may play a protective role against PWN infection-induced oxidative stress. Further, the biosynthesis of flavonoids, known to directly control parasitic nematodes, was commonly upregulated under SAR conditions. The ASM- and MeSA-specific expression patterns revealed functional branches for myricetin and quercetin production in flavonol biosynthesis. This study will enhance the understanding of the dynamic interactions between pine hosts and PWN under SAR conditions.
Keywords: Bursaphelenchus xylophilus; Pinus densiflora; acibenzolar-S-methyl (ASM); comparative transcriptome; methyl salicylic acid (MeSA); pine wilt disease; systemic acquired resistance (SAR).