Phytophthora cinnamomi is a globally significant plant pathogen, infecting over 5,000 plant species and posing substantial challenges to conventional management strategies (Hardham et al. 2018). Unlike most plant pathogens, Phytophthora species lack the ability to synthesize sterols de novo but retain key sterol-related genes, such as C-5 sterol desaturase and 7-dehydrocholesterol reductase. The functions of these genes and the role of sterols in the metabolism and pathogenicity of P. cinnamomi remain poorly understood (Kharel et al., 2021). As sterols are critical for cellular maintenance, homeostasis, and defense across eukaryotes, this dependency represents a potential vulnerability for innovative disease control strategies (Der et al. 2024).
Our research investigates the adaptive mechanisms of P. cinnamomi for sterol acquisition and the ability of the host plant to modulate sterol availability (Kharel et al., 2024a). On the pathogen side, we identified four sterol-sensing domain-containing proteins (SCPs) and multiple copies of elicitin genes in P. cinnamomi, which are critical for detecting and recruiting host sterols. Gene expression analyses revealed that sterol-sensing and recruitment genes are upregulated under sterol-deficient conditions, illustrating an adaptive strategy to enhance sterol acquisition. The retention of sterol-conversion enzymes highlights the preference of P. cinnamomi for Δ5-sterols, the predominant sterol type in plants.
On the host side, a soil-free Nicotiana benthamiana system was used to study the interaction between P. cinnamomi and plant sterol pathways, as well as the effects of phosphite treatment (Kharel et al. 2024b). Phosphite, a systemic chemical traditionally linked to plant defense activation, displayed dual functionality by modulating immune receptors and sterol biosynthesis. In the absence of phosphite, P. cinnamomi rapidly invaded N. benthamiana root cells, causing necrotic lesions and extensive pathogen spread. Infection led to a significant upregulation of sterol-related host genes, including the elicitin receptors REL and SOBIR, as well as CYP710A, which encodes a C22-sterol desaturase associated with increased pathogen susceptibility. Conversely, phosphite treatment reduced pathogen spread and disease severity. Despite infection, phosphite-treated hosts exhibited relatively low sterol-related gene expression, stabilizing sterol availability. This likely restricted pathogen proliferation while allowing the host additional time to activate defense mechanisms, contributing to disease suppression.
Our findings provide new insights into the sterol dependency of P. cinnamomi and its interactions with host sterol metabolism. By elucidating these molecular mechanisms, this research lays the groundwork for innovative sterol-targeted management strategies. Exploiting this dependency could offer a powerful tool for controlling this highly adaptable and destructive pathogen.