ABSTRACT
Phytophthora palmivora, a hemibiotrophic oomycete, causes diseases in several economically important tropical crops, such as oil palm, which it is responsible for a devastating disease called bud rot (BR). Despite recent progress in understanding host resistance and virulence mechanisms, many aspects remain unknown in P. palmivora isolates from oil palm. Model pathosystems are useful for understanding the molecular interactions between pathogens and hosts. In this study, we utilized detached leaves and whole seedlings of Arabidopsis thaliana Col-0 to describe and evaluate the infection process of three P. palmivora isolates (CPPhZC-05, CPPhZC-04, CPPhZOC-01) that cause BR in oil palm. Two compatible isolates (CPPhZC-05 and CPPhZOC-01) induced aqueous lesions at 72 h post-inoculation (hpi), with microscopic visualization revealing zoospore encysting and appressorium penetration at 3 hpi, followed by sporangia generation at 72 hpi. In contrast, an incompatible isolate (CPPhZC-04) exhibited cysts that could not penetrate tissue, resulting in low leaf colonization. Gene expression of ten P. palmivora infection-related genes was quantified by RT-qPCR, revealing overexpression in compatible isolates, but not in the incompatible isolate. Additionally, key genes associated with salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) in Arabidopsis exhibited regulation during interaction with the three isolates. These findings demonstrate that P. palmivora can infect Arabidopsis Col-0, and variability is observed in the interaction between Arabidopsis-Col-0 and P. palmivora isolates. Establishing this pathosystem is expected to enhance our understanding of P. palmivora's pathology and physiology.
ABSTRACT
Bud Rot, caused by Phytophthora palmivora, is considered one of the main diseases affecting African oil palm (Elaeis guineensis). In this study, we investigated the in vitro molecular dynamics of the pathogen-host interaction by analyzing gene expression profiles from oil palm genotypes that were either susceptible or resistant to the disease. We observed distinct interactions of P. palmivora with resistant and susceptible oil palms through co-expression network analysis. When interacting with susceptible genotypes, P. palmivora exhibited upregulation of carbohydrate and sulfate transport genes. These genes demonstrated co-expression with apoplastic and cytoplasmic effectors, including cell wall degrading enzymes, elicitins, and RxLR motif effectors. The pathogen manipulated susceptible oil palm materials, exacerbating the response and compromising the phenylpropanoid pathway, ultimately leading to susceptibility. In contrast, resistant materials exhibited control over their response through putative Heat Shock Proteins (HSP) that maintained homeostasis between primary metabolism and biotic defense. Co-expressed genes related to flavonoids, WRKY transcripts, lectin-type receptors, and LRR receptors may play important roles in pathogen control. Overall, the study provides new knowledge of the molecular mechanisms underlying the interaction between E. guineensis and P. palmivora, which can contribute to controlling Bud Rot in oil palms and gives new insights into the interactions of P. palmivora with their hosts.