Certain obligate parasites induce complex and substantial phenotypic changes in their hosts in ways that favor their transmission to other trophic levels. However, the mechanisms underlying these changes remain largely unknown. Here we demonstrate how SAP05 protein effectors from insect-vectored plant pathogenic phytoplasmas take control of several plant developmental processes. These effectors simultaneously prolong the host lifespan and induce witches’ broom-like proliferations of leaf and sterile shoots, organs colonized by phytoplasmas and vectors. SAP05 acts by mediating the concurrent degradation of SPL and GATA developmental regulators via a process that relies on hijacking the plant ubiquitin receptor RPN10 independent of substrate ubiquitination. RPN10 is highly conserved among eukaryotes, but SAP05 does not bind insect vector RPN10. A two-amino-acid substitution within plant RPN10 generates a functional variant that is resistant to SAP05 activities. Therefore, one effector protein enables obligate parasitic phytoplasmas to induce a plethora of developmental phenotypes in their hosts.

某些专性寄生虫以有利于其传播到其他营养级的方式诱导其宿主发生复杂且实质性的表型变化。然而，这些变化背后的机制仍然很大程度上未知。在这里，我们展示了来自昆虫媒介植物病原植原体的 SAP05 蛋白效应子如何控制多个植物发育过程。这些效应子同时延长宿主的寿命，并诱导叶和不育芽、植原体和载体定植的器官的扫帚式增殖。 SAP05 通过依赖于劫持植物泛素受体 RPN10 的过程介导 SPL 和 GATA 发育调节因子的同时降解，而与底物泛素化无关。 RPN10 在真核生物中高度保守，但 SAP05 不结合昆虫载体 RPN10。植物 RPN10 内的两个氨基酸取代产生了对 SAP05 活性具有抵抗力的功能变体。因此，一种效应蛋白使专性寄生植原体能够在宿主中诱导多种发育表型。