An effector of the Irish potato famine pathogen antagonizes a host autophagy cargo receptor.

Plants and other living organisms can survive stress and starvation by digesting and recycling parts of their own cells. This process is known as autophagy and it involves engulfing cellular material inside spherical structures called autophagosomes, before delivering it to sites in the cell where digestive enzymes can break the material down. A form of autophagy, known as selective autophagy, can specifically degrade toxic substances such as disease-causing microbes. Selective autophagy works through proteins called autophagy cargo receptors that define which molecules are targeted for degradation. However, it was not clear whether autophagy protects plants from infections, or how much disease-causing microbes interfere with this process for their own benefit. The microbe that causes late blight of potatoes (called Phytophthora infestans) is infamous for triggering widespread famines in Ireland in the 19th century. This disease-causing microbe continues to pose a serious threat to food security today, and parasitizes plant tissues by releasing proteins called effectors that enter the plant’s cells to subvert the plant’s physiology and counteract its defenses. Dagdas, Belhaj et al. now report that an effector from P. infestans, called PexRD54, can bind to autophagy-related protein from potato, called ATG8CL, and stimulate the formation of autophagosomes. Further experiments revealed that the PexRD54 effector could outcompete a plant autophagy cargo receptor that would otherwise bind to ATG8CL. This plant cargo receptor contributes to the plant’s defences, and by preventing it from interacting with ATG8CL, PexRD54 makes the plant more susceptible to infection by P. infestans. These findings show that the PexRD54 effector has evolved to interact with an autophagy-related protein to counteract the plant’s defences. Dagdas, Belhaj et al. suggest that PexRD54 might do this by activating autophagy to selectively eliminate some of the molecules that the plant use to defend itself. Furthermore, P. infestans might also benefit from the nutrients that are released when cellular material is broken down via autophagy. Future work could test these two hypotheses and explore whether other effectors from disease-causing microbes work in a similar way.