Wang Juanping, Wang Chang, Li Qi, Shen Mengyuan, Bai Peng, Li Jionghui, Lin Yan, Gan Nanqin, Li Tao, Zhao Jindong
State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.
University of Chinese Academy of Sciences, Beijing, China.
Front Microbiol. 2019 Aug 6;10:1750. doi: 10.3389/fmicb.2019.01750. eCollection 2019.
The bacterium sp. THN1 (THN1) is capable of degrading microcystin-LR (MC-LR). To study the ability of THN1 to degrade MC-LR and its possible mechanism(s) of regulation, we analyzed the effect of carbon concentrations on the degradation process. The MC-LR degradation rate peaked early and then declined during MC-LR biodegradation. Decreased levels of carbon in the medium caused the degradation peak to occur earlier. The expression of the functional gene , encoding a microcystinase, showed a similar trend to the MC-LR degradation rate at various carbon concentrations (r = 0.717, < 0.05), suggesting that regulation of expression may play an important role in MC-LR degradation by THN1. The total bacterial biomass decreased when the carbon source was limited and did not correlate with the MC-LR degradation rate. Transcriptomic analysis showed that MC-LR degradation differentially regulated 62.16% (2597/4178) of THN1 genes. A considerable number of differentially expressed genes (DEGs) during MC-LR degradation encoded proteins related to carbon-, nitrogen-, and amino acid-related pathways. At 2 h of MC-LR degradation, most DEGs (29/33) involved in carbon and nitrogen metabolism were downregulated. This indicated that MC-LR may regulate carbon and nitrogen pathways of sp. THN1. KEGG pathway analysis indicated that the upregulated DEGs during MC-LR degradation were mainly related to amino acid degradation and substrate metabolism pathways. Particularly, we detected increased expression of glutathione metabolism-related genes from transcriptomic data at 2 h of MC-LR degradation compared with the gene expression of 0 h, such as GST family protein, glutathione peroxidase, S-(hydroxymethyl) glutathione dehydrogenase, and glutathione-dependent disulfide-bond oxidoreductase that have been reported to be involved in microcystin degradation.
菌株THN1能够降解微囊藻毒素-LR(MC-LR)。为了研究THN1降解MC-LR的能力及其可能的调控机制,我们分析了碳浓度对降解过程的影响。在MC-LR生物降解过程中,MC-LR降解率先达到峰值,然后下降。培养基中碳含量的降低导致降解峰值提前出现。编码微囊藻毒素酶的功能基因的表达在不同碳浓度下与MC-LR降解率呈现相似趋势(r = 0.717,P < 0.05),表明该基因表达的调控可能在THN1降解MC-LR过程中起重要作用。当碳源有限时,细菌总生物量下降,且与MC-LR降解率无关。转录组分析表明,MC-LR降解差异调控了THN1基因的62.16%(2597/4178)。MC-LR降解过程中有相当数量的差异表达基因(DEGs)编码与碳、氮和氨基酸相关途径的蛋白质。在MC-LR降解2小时时,参与碳和氮代谢的大多数DEGs(29/33)被下调。这表明MC-LR可能调控THN1菌株的碳和氮途径。KEGG通路分析表明,MC-LR降解过程中上调的DEGs主要与氨基酸降解和底物代谢途径相关。特别是,与0小时的基因表达相比,我们在转录组数据中检测到MC-LR降解2小时时谷胱甘肽代谢相关基因的表达增加,如GST家族蛋白、谷胱甘肽过氧化物酶、S-(羟甲基)谷胱甘肽脱氢酶和谷胱甘肽依赖性二硫键氧化还原酶,这些基因已被报道参与微囊藻毒素的降解。