Analysis reveals TCP impact on virulence functions and host specificity in phytoplasma, suggesting adaptive evolution may evade immune responses.
Remarkable phenotypic plasticity of phytoplasma infections stems from the fast evolution and functional divergence of a versatile effector arsenal. We first catalogue more than 50 characterised effectors, highlighting their interference with SPL/GATA, TCP, MADS‐box and ARF hubs, and the combined consequences for plant morphogenesis, hormone homoeostasis and vector colonisation. We then explain how drastic genome reduction coexists with extensive repeats and is balanced by PMU‐mediated replication and recombination to maintain genetic flexibility. Comparisons at the population level indicate that most effectors are located on PMUs, which promote the evolution of effectors through recombination, replication and horizontal transfer. Purifying selection preserves essential virulence functions and eliminates mutations that compromise effector activity, while diversifying selection fine‐tunes host specificity and may aid evasion of host immune responses. Finally, we argue that elucidating the mechanistic link between the dynamics of PMUs and effector evolution may provide deeper insights into the molecular mechanisms of host manipulation.
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Gan et al. (2025) studied this question.
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