Salt stress substantially leads to flowering delay. The regulation of salt‐induced late flowering has been studied at the transcriptional and protein levels; however, the involvement of secondary metabolites has rarely been investigated. Here, we report that FMOGS‐OXs (EC 1.14.13.237), the enzymes that catalyze the biosynthesis of glucosinolates (GSLs), promote flowering transition in Arabidopsis thaliana. It has been reported that WRKY75 is a positive regulator, and MAF4 is a negative regulator of flowering transition. The products of FMOGS‐OXs, methylsulfinylalkyl GSLs (MS GSLs), facilitate flowering by inducing WRKY75 and repressing the MAS‐MAF4 module. We further show that the degradation of MS GSLs is involved in salt‐induced late flowering and salt tolerance. Salt stress induces the expression of myrosinase genes, resulting in the degradation of MS GSLs, thereby relieving the promotion of WRKY75 and inhibition of MAF4, leading to delayed flowering. In addition, the degradation products derived from MS GSLs enhance salt tolerance. Previous studies have revealed that FMOGS‐OXs exhibit alternative catalytic activity to form trimethylamine N‐oxide (TMAO) under salt stress, which activates multiple stress‐related genes to promote salt tolerance. Therefore, FMOGS‐OXs integrate flowering transition and salt tolerance in various ways. Our study shed light on the functional diversity of GSLs and established a connection between flowering transition, salt resistance, and GSL metabolism.

中文翻译：

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含黄素单加氧酶 FMOGS-OXs 整合拟南芥开花转变和耐盐性

盐胁迫严重导致开花延迟。盐诱导晚花的调节已在转录和蛋白质水平上进行了研究；然而，很少研究次生代谢物的参与。在此，我们报告 FMOGS-OXs (EC 1.14.13.237)，催化硫代葡萄糖苷 (GSL) 生物合成的酶，促进开花过渡拟南芥。据报道，WRKY75是开花过渡的正调节因子，MAF4是开花过渡的负调节因子。 FMO的产品GS-OXs，甲基亚磺酰烷基 GSL（MS GSL），通过诱导促进开花WRKY75并压制新加坡金融管理局‐MAF4模块。我们进一步表明，MS GSL 的降解与盐诱导的晚花和耐盐性有关。盐胁迫诱导黑芥子酶基因表达，导致MS GSLs降解，从而缓解促进WRKY75和抑制MAF4，导致开花延迟。此外，MS GSL 产生的降解产物增强了耐盐性。此前的研究表明，FMOGS-OX在盐胁迫下，它们表现出替代催化活性，形成三甲胺 N-氧化物（TMAO），从而激活多个与胁迫相关的基因以促进耐盐性。因此，FMOGS-OX以多种方式整合开花过渡和耐盐性。我们的研究揭示了 GSL 的功能多样性，并建立了开花转变、耐盐性和 GSL 代谢之间的联系。