Table_1_Comparative transcriptome profiling reveals the importance of GmSWEET15 in soybean susceptibility to Sclerotinia sclerotiorum.XLSX

Soybean sclerotinia stem rot (SSR) is a disease caused by Sclerotinia sclerotiorum that causes incalculable losses in soybean yield each year. Considering the lack of effective resistance resources and the elusive resistance mechanisms, we are urged to develop resistance genes and explore their molecular mechanisms. Here, we found that loss of GmSWEET15 enhanced the resistance to S. sclerotiorum, and we explored the molecular mechanisms by which gmsweet15 mutant exhibit enhanced resistance to S. sclerotiorum by comparing transcriptome. At the early stage of inoculation, the wild type (WT) showed moderate defense response, whereas gmsweet15 mutant exhibited more extensive and intense transcription reprogramming. The gmsweet15 mutant enriched more biological processes, including the secretory pathway and tetrapyrrole metabolism, and it showed stronger changes in defense response, protein ubiquitination, MAPK signaling pathway-plant, plant-pathogen interaction, phenylpropanoid biosynthesis, and photosynthesis. The more intense and abundant transcriptional reprogramming of gmsweet15 mutant may explain how it effectively delayed colonization by S. sclerotiorum. In addition, we identified common and specific differentially expressed genes between WT and gmsweet15 mutant after inoculation with S. sclerotiorum, and gene sets and genes related to gmsweet15_24 h were identified through Gene Set Enrichment Analysis. Moreover, we constructed the protein–protein interaction network and gene co-expression networks and identified several groups of regulatory networks of gmsweet15 mutant in response to S. sclerotiorum, which will be helpful for the discovery of candidate functional genes. Taken together, our results elucidate molecular mechanisms of delayed colonization by S. sclerotiorum after loss of GmSWEET15 in soybean, and we propose novel resources for improving resistance to SSR.

大豆菌核茎腐病（Soybean sclerotinia stem rot, SSR）是由核盘菌（Sclerotinia sclerotiorum）引发的病害，每年均可对大豆产量造成难以估量的损失。鉴于目前缺乏有效的抗病资源且抗病机制尚不明确，亟需挖掘抗病基因并解析其分子作用机制。本研究发现，GmSWEET15功能缺失可增强大豆对核盘菌的抗性；随后通过转录组（transcriptome）比较分析，解析了gmsweet15突变体增强核盘菌抗性的分子机制。在接种早期，野生型（Wild type, WT）仅表现出中等强度的防御响应，而gmsweet15突变体则呈现出更为广泛且强烈的转录重编程（transcription reprogramming）。gmsweet15突变体富集了更多的生物学过程，包括分泌通路与四吡咯代谢；同时在防御响应、蛋白质泛素化、MAPK信号通路-植物（MAPK signaling pathway-plant）、植物-病原互作、苯丙烷生物合成以及光合作用等通路中呈现出更为显著的表达变化。gmsweet15突变体更为强烈且丰富的转录重编程，或可解释其为何能有效延缓核盘菌的定殖过程。此外，本研究鉴定了接种核盘菌后野生型与gmsweet15突变体之间的共有与特异性差异表达基因，并通过基因集富集分析（Gene Set Enrichment Analysis, GSEA）筛选得到了与gmsweet15_24 h相关的基因集与功能基因。进一步，本研究构建了蛋白质-蛋白质相互作用网络与基因共表达网络，筛选得到多组gmsweet15突变体响应核盘菌的调控网络，这将为候选功能基因的挖掘提供重要依据。综上，本研究阐明了大豆GmSWEET15功能缺失后延缓核盘菌定殖的分子机制，并为大豆菌核茎腐病（SSR）的抗病性改良提供了全新的基因资源。