ABSTRACT Clubroot, caused by the soil‐borne protist Plasmodiophora brassicae , is a major disease of Brassica crops, resulting in severe root malformations and yield losses. While most research has centred on immune signalling and hormone dynamics, plant–pathogen interactions also dramatically reshape primary metabolism, often modifying source activity and converting infected tissues into strong metabolic sinks. The SnRK1 (SNF1‐related kinase 1) protein kinase acts as a cellular fuel gauge in plants, integrating metabolic status and environmental and developmental cues to maintain carbon and energy homoeostasis. Here, we explored SnRK1‐mediated quantitative resistance against clubroot disease in the related crucifer model Arabidopsis thaliana . Both soil‐ and hydroponics‐based disease assays revealed how especially increased nuclear SnRK1α1 activity antagonizes clubroot development, suggesting a pivotal role for transcriptional regulation. qRT‐PCR analysis and quantification of soluble sugar contents and invertase activity in roots indicate that SnRK1‐mediated resistance coincides with reduced sucrose transporter expression as well as cell wall invertase expression and activity, likely limiting clubroot development by reducing sink strength. Consistently, cellular assays indicate that the recently identified SnRK1α1‐targeting P. brassicae effector PBZF1 interferes with SnRK1α1 nuclear translocation. Our study thus corroborates that SnRK1 is a primary effector target and shows that SnRK1‐mediated reprogramming of gene expression and sink activity is an effective mechanism against clubroot disease development.
Vijayakumar et al. (Tue,) studied this question.