Extended phenotype of phytoplasmas in eukaryotic systems: mechanisms and ecological implications

Manipulation of host behavior is believed to result from parasitic genes influencing the host's genes or its environment. This adaptive strategy, known as an extended phenotype, boosts the fitness and adaptation of pathogens. Numerous examples of extended phenotypes exist in nature, including zombie ants, fearless mice, brood parasitism in cuckoos, and zombie spiders, some of which are discussed in this review. In certain cases, parasitic pathogens cause morphological changes in their hosts that directly benefit the parasites by enhancing their adaptive fitness. Notably, plant pathogens, such as phytoplasmas, display extended phenotypes on hosts and insect vectors through the secretion of effector proteins like SAP54, PHYL1, SAP11, SAP05, TENGU, SWP1, SJP1, SJP2, Zaofeng3 (SJP3), SJP39, and Zaofeng6. These effector proteins are key factors in producing phenotypic changes in host plants that increase plant attractiveness to leafhopper vectors by targeting and degrading key transcription factors and developmental regulators. This process aligns with the concept of extended phenotype, as it significantly improves the adaptive fitness of phytoplasmas. This review explores the extended phenotype of phytoplasmas on dual eukaryotic hosts, focusing on effector proteins, their mechanisms, and modern strategies to counteract them.