Dual RNA-seq analysis unveils the molecular interactions between coconut (Cocos nucifera L.) and Phytophthora palmivora, the bud rot pathogen

Abstract

Background The bud rot pathogen Phytophthora palmivora poses a significant threat to coconut production worldwide. Effective management strategies against this devastating pathogen are lacking due to the absence of resistant cultivars and limited knowledge about its pathogenicity mechanisms. To address this, we conducted dual RNA-seq analyses at three time points (12, 24, and 36 hours post-infection) during the initial progression of the disease, using a standardized in vitro assay. This study aimed to identify transcriptional regulation following infection and decipher the system-level host response to P. palmivora. Results Differential gene expression (DGE) analysis between control and infected samples revealed extensive modulation of stress-responsive genes in coconut. In contrast, P. palmivora showed differential expression of genes encoding effector and carbohydrate-active enzymes (CAZy). Pathway enrichment analysis highlighted the up-regulation of genes associated with plant-pathogen interaction pathway and plant hormone signal transduction in coconut. To validate our findings, we selected ten candidate differentially expressed genes (DEGs) from both coconut and P. palmivora for quantification using qRT-PCR at the three time points. The expression trends observed in qRT-PCR confirmed the reliability of the dual RNA-seq data, further supporting the comprehensive outlook on the global response of coconut to P. palmivora infection. Conclusions This study highlights the significant modulation of stress-responsive genes in coconut and differential expression of effector and carbohydrate-active enzyme genes in P. palmivora during bud rot infection. The findings provide valuable insights into the molecular interactions and transcriptional regulation underlying the coconut-P. palmivora pathosystem, aiding in the development of effective management strategies against this devastating pathogen.