Genome-wide transcriptome profiles reveal how Bacillus subtilis lipopeptides inhibit microsclerotia formation in Verticillium dahliae
Genome-wide transcriptome profiles reveal how Bacillus subtilis lipopeptides inhibit microsclerotia formation in Verticillium dahliae
复制标题
全基因组转录组图谱揭示了枯草芽孢杆菌脂肽如何抑制大丽黄萎病菌中微菌核的形成
DOI:
10.1094/mpmi-08-18-0233-r
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发表时间:
2018
影响因子:
3.5
通讯作者:
Wang Yonglin
中科院分区:
文献类型:
--
作者:
Yu Dimei;Fang Yulin;Tang Chen;Klosterman Steven;Tian Chengming;Wang Yonglin
Verticillium dahliaeis a soilborne fungus and the primary causal agent of vascular wilt diseases worldwide. The fungus produces melanized microsclerotia that are crucially important for the survival and spread ofV. dahliae. There are no fungicides available that are both effective and environmentally friendly to suppress the fungus. Previously,Bacillus subtilisC232 was isolated from soil and was demonstrated to suppress microsclerotia formation inV. dahliae. In this study, liquid chromatography coupled with mass spectrometry revealed that the antifungal substance is actually a mixture of lipopeptides. Exposure ofV. dahliaeto these lipopeptides resulted in hyphal swelling, cell lysis, and downregulation of melanin-related genes. RNA sequencing analyses of the lipopeptide-suppressed transcriptome during microsclerotial development revealed that 5,974 genes (2,131 upregulated and 3,843 downregulated) were differentially expressed versus nonsuppressive conditions. Furthermore, gene ontology enrichment analyses revealed that genes involved in response to stress, cellular metabolic processes, and translation were significantly enriched. Additionally, the lipopeptides inhibited expression of genes associated with secondary metabolism, protein catabolism, and the high-osmolarity glycerol response signaling pathway. Together, these findings provide evidence for the mechanism by whichB. subtilislipopeptides suppress microsclerotia formation. The transcriptomic insight garnered here may facilitate the development of biological agents to combat Verticillium wilt.