College of Horticulture, College of Life Sciences, FAFU-UCR Joint Center for Horticultural Biology and Metabolomics, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing 210095, China.
Plant Cell. 2022 Sep 27;34(10):4045-4065. doi: 10.1093/plcell/koac212.
Forming mutualistic symbioses with arbuscular mycorrhizae (AMs) improves the acquisition of mineral nutrients for most terrestrial plants. However, the formation of AM symbiosis usually occurs under phosphate (Pi)-deficient conditions. Here, we identify SlSPX1 (SYG1 (suppressor of yeast GPA1)/Pho81(phosphate 81)/XPR1 (xenotropic and polytropic retrovirus receptor 1) as the major repressor of the AM symbiosis in tomato (Solanum lycopersicum) under phosphate-replete conditions. Loss of SlSPX1 function promotes direct Pi uptake and enhances AM colonization under phosphate-replete conditions. We determine that SlSPX1 integrates Pi signaling and AM symbiosis by directly interacting with a set of arbuscule-induced SlPHR proteins (SlPHR1, SlPHR4, SlPHR10, SlPHR11, and SlPHR12). The association with SlSPX1 represses the ability of SlPHR proteins to activate AM marker genes required for the arbuscular mycorrhizal symbiosis. SlPHR proteins exhibit functional redundancy, and no defective AM symbiosis was detected in the single mutant of SlPHR proteins. However, silencing SlPHR4 in the Slphr1 mutant background led to reduced AM colonization. Therefore, our results support the conclusion that SlSPX1-SlPHRs form a Pi-sensing module to coordinate the AM symbiosis under different Pi-availability conditions.
与丛枝菌根（AM）形成互利共生关系可以改善大多数陆生植物对矿质养分的获取。然而，AM 共生的形成通常发生在缺磷（Pi）的条件下。在这里，我们确定 SlSPX1（SYG1（酵母 GPA1 的抑制剂）/Pho81（磷酸 81）/XPR1（异嗜性和多嗜性逆转录病毒受体 1））是番茄（Solanum lycopersicum）在磷充足条件下 AM 共生的主要抑制因子。SlSPX1 功能的丧失促进了在磷充足条件下直接 Pi 吸收和 AM 定殖。我们确定 SlSPX1 通过直接与一组丛枝诱导的 SlPHR 蛋白（SlPHR1、SlPHR4、SlPHR10、SlPHR11 和 SlPHR12）相互作用，整合 Pi 信号和 AM 共生。与 SlSPX1 的关联抑制了 SlPHR 蛋白激活丛枝菌根共生所需的 AM 标记基因的能力。SlPHR 蛋白具有功能冗余性，在单个 SlPHR 蛋白突变体中未检测到缺陷型 AM 共生。然而，在 Slphr1 突变体背景下沉默 SlPHR4 导致 AM 定殖减少。因此，我们的结果支持 SlSPX1-SlPHRs 形成 Pi 感应模块的结论，该模块可以在不同 Pi 可利用条件下协调 AM 共生。
