Effector biology during biotrophic invasion of plant cells

Chaudhari, Prateek; Ahmed, Bulbul; Joly, David L; Germain, Hugo

Nuclear effectors are seemingly ultimate weapons in the inventory of pathogens, since they are thought to suppress the immune response from upstream. Nuclear effectors could potentially shut off master switches of the immune machinery or reprogram host transcription to the benefit of pathogens. A recent investigation of 49 putative effectors from H. arabidopsidis revealed that 33% localized strictly to the nucleus, and an additional 33% were nucleo-cytoplasmic. 30 Since several effectors tend to migrate toward the nucleus, it would be logical to assume that some R-proteins act in the nucleus. Indeed, several R-proteins, such as SNC1, N and RPS4, were found to localize to the nucleus. [31] [32] [33] [34] Tobacco TIR-NB-LRR R-protein N localizes to the nucleus in the absence of its elicitor, the Tobacco mosaic virus p50 helicase fragment, 32 lending support to a default presence of R-proteins in the nucleus to monitor their corresponding effectors rather than being relocalized upon effector binding. However, SNC1 and N nuclear accumulation is reduced at elevated temperatures, making their mode of action temperature-dependent. 35 It was demonstrated recently that ETI is more active at low temperatures (10-23 °C), while PTI takes over at higher temperatures (23-32 °C) . 36 It has also been shown that bacterial pathogens strive and multiply at higher temperatures but secrete their effectors more actively at lower temperatures. 37, 38 These observations suggest that the immune system of plants is adapted to pathogen physiology. However, some pathogens prefer more temperate environments (around 18 °C) for optimal growth. 39,40