Metabolomics and WGCNA Analyses Reveal the Underlying Mechanisms of Resistance to Botrytis cinerea in Hazelnut

Hazelnut (Corylus), a significant woody oil tree species in economic forests, faces production constraints due to biotic stresses, with Hazelnut Husk Brown Rot, caused by the pathogenic necrotrophic fungus Botrytis cinerea (B. cinerea), being the most severe. To date, limited information is available regarding the resistance of hazelnuts to B. cinerea. To better understand the mechanisms of resistance to B. cinerea. in hazelnut, we conducted metabolomics and WGCNA analyses of a B. cinerea-resistant Ping'ou hybrid hazelnut variety (Dawei; DW) and a susceptible variety (Qiuxiang; QX).

This study provides that the elevated levels of these compounds (flavonoids and phenolic acids) contribute substantially to the resistance of hazelnut against B. cinerea. Furthermore, 3,4-hydroxyphenyllactic acid and phloretin were identified as pivotal metabolites in modulating the resistance of hazelnut to B. cinerea. Through WGCNA analyses, we identified four transcription factors (WRKY19, HSFC1, ERF071, and RAP2-1) that are most likely to regulate the synthesis of 3,4-dihydroxyphenyllactic acid and phloretin. This study provides crucial insights for further investigation into the regulatory network of metabolites associated with hazelnut resistance to B. cinerea.

In this study, metabolomics and weighted gene co-expression network analysis (WGCNA, weighted correlation network analysis) were applied to elucidate the resistance mechanisms underlying different hazelnut varieties to B. cinerea. Our study focused on the metabolome profiles of DW and QX plants after 72 h of B. cinerea infection.

Venn analysis of QX_0 vs. DW_0 and QX_72 vs. DW_72 revealed 120 differential accumulation metabolites (DAMs) that were upregulated. Among these metabolites, the concentrations of flavonoids and phenolic acids in DW were significantly higher than those in QX, respectively, suggesting that the elevated levels of these compounds contribute substantially to the resistance of hazelnut against B. cinerea. 3,4-hydroxyphenyllactic acid and phloretin were significantly more abundant in accumulation in DW than in QX after infection by B. cinerea. Conclusions: This study provides that the elevated levels of these compounds (flavonoids and phenolic acids) contribute substantially to the resistance of hazelnut against B. cinerea. Furthermore, 3,4-hydroxyphenyllactic acid and phloretin were identified as pivotal metabolites in modulating the resistance of hazelnut to B. cinerea. Through WGCNA analyses, we identified four transcription factors (WRKY19, HSFC1, ERF071, and RAP2-1) that are most likely to regulate the synthesis of 3,4-dihydroxyphenyllactic acid and phloretin. This study provides crucial insights for further investigation into the regulatory network of metabolites associated with hazelnut resistance to B. cinerea.