Fujian Key Laboratory of Marine Enzyme Engineering, College of Biological Science and Engineering, Fuzhou University, Fuzhou, Fujian 350116, China.
Fujian Key Laboratory of Marine Enzyme Engineering, College of Biological Science and Engineering, Fuzhou University, Fuzhou, Fujian 350116, China.
J Invertebr Pathol. 2021 May;181:107564. doi: 10.1016/j.jip.2021.107564. Epub 2021 Mar 6.
Beauveria bassiana is a critical entomopathogenic fungus for pest biocontrol, whose efficiency depends on fungal development and stress resistance. Unlike its revealed location in plasma membrane patches in other organisms, B. bassiana Sur7 specifically localized in vacuoles. This vacuolar Sur7 was previously demonstrated to affect stress tolerance, hyphal development and virulence. There, however, remain more mechanistic details to be explored. In this study, transcriptomics and metabolomics were applied to investigate the mechanism of vacuolar Sur7. Analyses of transcriptomics and metabolomics displayed many differentially expressed genes and abundant metabolites in response to Sur7 loss, respectively. Together with genes associated with vacuolar biofunction (including transportation and hydrolysis), the altered metabolites contributed to cell wall construction and stress resistance. Particularly, an N-acetylglucosamine-associated Brg1/Nrg1 pathway was enriched and partially affected by Sur7. Absence of Sur7 changed the expression level of Brg1/Nrg1 pathway-related transcript factors, which interfered with downstream phenotype of sporulation. In addition, Sur7 was involved in the accumulation of sphingoid bases, which may affect sphingolipid-related signaling pathway. Although experimental evidence is further required, our studies provide a preliminary framework for future exploring the regulatory mechanism of Sur7, and give a new version of metabolic agency connecting Sur7 and downstream signaling pathway.
球孢白僵菌是一种重要的昆虫病原真菌，可用于害虫的生物防治，其效率取决于真菌的发育和抗逆能力。与在其他生物体中发现的位于质膜斑中的位置不同，球孢白僵菌 Sur7 特异性定位于液泡中。先前的研究表明，液泡中的 Sur7 会影响其应激耐受性、菌丝发育和毒力。然而，其中仍有更多的机制细节需要探索。在这项研究中，我们应用转录组学和代谢组学来研究液泡 Sur7 的作用机制。转录组学和代谢组学的分析分别显示了许多差异表达基因和大量与 Sur7 缺失相关的代谢物。与液泡生物功能相关的基因（包括运输和水解）一起，改变的代谢物有助于细胞壁的构建和应激抵抗。特别是，富含与 N-乙酰葡萄糖胺相关的 Brg1/Nrg1 途径，并被 Sur7 部分影响。Sur7 的缺失改变了 Brg1/Nrg1 途径相关转录因子的表达水平，干扰了孢子形成的下游表型。此外，Sur7 还参与了鞘氨醇碱基的积累，这可能会影响鞘脂相关信号通路。尽管需要进一步的实验证据，但我们的研究为未来探索 Sur7 的调控机制提供了一个初步的框架，并为连接 Sur7 和下游信号通路的代谢机制提供了一个新的版本。
