Aims To explore the mechanisms of continuous cropping obstacles of tobacco using co-occurrence network analyses to identify interactions between rhizosphere soil microbiota and metabolites. Methods Using pot experiments, tobacco biomass, soil chemical properties were routinely determined over three continuous growth seasons. Rhizosphere microbiota and metabolites were respectively determined using phospholipid fatty acids (PLFAs) and gas chromatography-mass spectrometry, and then analysed using co-occurrence network analyses to explore growth obstacle mechanisms of tobacco. Results Tobacco biomass was significantly lower in the 2nd- and 3rd-season soils when compared with soils from the 1st-season – indicating growth obstacles. Three PLFA biomarkers (a16:0, 17:1ω8c, and 20:0) and five (i14:0, i15:1G, 17:0, 11Me18:1ω7c, and 16:1ω5c) were distinct to the 2nd- and 3rd-season soils, respectively. In the 2nd-season, 33 metabolites (phenol, cyclopropanebutanoic acid, 16-octadecenoic acid, n-hexadecanoic acid, and [z]-13-docosenamide, etc.) were up-regulated, and 10 metabolites ( d -(−)-ribofuranose, d -(+)-cellobiose, and myo-inositol, etc.) down-regulated. Co-occurrence network analyses indicated that 16-octadecenoic acid, n-hexadecanoic acid, oleic acid and [z]-13-docosenamide might act as “hubs” to alter the secondary metabolism, d -(−)-ribofuranose and d -(+)-cellobiose as key metabolites to induce the changes in microbial compositions, while myo-inositol as a “trigger” metabolite in negative feedback signaling between plants and microbes. Conclusion We found that a combination of positive feedback involving allelochemicals (i.e. phenolic acids) and negative feedback involving metabolites (i.e. myo-inositol, D-(−)-ribofuranose and D-(+)-cellobiose) could result in changes to soil microbial composition associated with plant growth obstacles.

中文翻译：

---

烟草连作季节根际土壤微生物PLFAs及其代谢物共生网络分析

目的 利用共生网络分析确定根际土壤微生物群与代谢物之间的相互作用，探索烟草连作障碍的机制。方法使用盆栽试验，在三个连续生长季节中常规测定烟草生物量、土壤化学性质。分别使用磷脂脂肪酸 (PLFA) 和气相色谱-质谱法测定根际微生物群和代谢物，然后使用共生网络分析来探索烟草的生长障碍机制。结果 与第 1 季土壤相比，第 2 季和第 3 季土壤中的烟草生物量显着降低，表明存在生长障碍。三个 PLFA 生物标志物（a16:0、17:1ω8c 和 20:0）和五个（i14:0、i15:1G、17:0、11Me18:1ω7c 和 16：1ω5c) 分别与第 2 季和第 3 季土壤不同。第二季，33种代谢物（苯酚、环丙烷丁酸、16-十八碳烯酸、正十六烷酸、[z]-13-二十二碳素酰胺等）上调，10种代谢物（d-（-） -呋喃核糖、d -(+)-纤维二糖和肌醇等）下调。共生网络分析表明，16-十八碳烯酸、正十六烷酸、油酸和 [z]-13-二十二碳烯酰胺可能充当“枢纽”来改变次级代谢，d-(-)-呋喃核糖和 d-( +)-纤维二糖作为诱导微生物组成变化的关键代谢物，而肌醇作为植物和微生物之间负反馈信号中的“触发”代谢物。结论 我们发现涉及化感物质的正反馈组合（即