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磷脂酶D和磷脂酸介导灵芝热应激诱导的次生代谢。

Phospholipase D and phosphatidic acid mediate heat stress induced secondary metabolism in Ganoderma lucidum.

作者信息

Liu Yong-Nan, Lu Xiao-Xiao, Chen Dai, Lu Ya-Ping, Ren Ang, Shi Liang, Zhu Jing, Jiang Ai-Liang, Yu Han-Shou, Zhao Ming-Wen

机构信息

Key Laboratory of Agricultural Environmental Microbiology, Ministry of Agriculture, Microbiology Department, College of Life Sciences, Nanjing Agricultural University, Jiangsu, Nanjing 210095, People's Republic of China.

Biological experiment teaching center, College of Life Sciences, Nanjing Agricultural University, Nanjing 210095, People's Republic of China.

出版信息

Environ Microbiol. 2017 Nov;19(11):4657-4669. doi: 10.1111/1462-2920.13928. Epub 2017 Sep 21.

Abstract

Phospholipid-mediated signal transduction plays a key role in responses to environmental changes, but little is known about the role of phospholipid signalling in microorganisms. Heat stress (HS) is one of the most important environmental factors. Our previous study found that HS could induce the biosynthesis of the secondary metabolites, ganoderic acids (GA). Here, we performed a comprehensive mass spectrometry-based analysis to investigate HS-induced lipid remodelling in Ganoderma lucidum. In particular, we observed a significant accumulation of phosphatidic acid (PA) on HS. Further genetic tests in which pld-silencing strains were constructed demonstrated that the accumulation of PA is dependent on HS-activated phospholipase D (PLD) hydrolysing phosphatidylethanolamine. Furthermore, we determined the role of PLD and PA in HS-induced secondary metabolism in G. lucidum. Exogenous 1-butanol, which decreased PLD-mediated formation of PA, reverses the increased GA biosynthesis that was elicited by HS. The pld-silenced strains partly blocked HS-induced GA biosynthesis, and this block can be reversed by adding PA. Taken together, our results suggest that PLD and PA are involved in the regulation of HS-induced secondary metabolism in G. lucidum. Our findings provide key insights into how microorganisms respond to heat stress and then consequently accumulate secondary metabolites by phospholipid remodelling.

摘要

磷脂介导的信号转导在对环境变化的响应中起关键作用,但关于磷脂信号在微生物中的作用却知之甚少。热应激(HS)是最重要的环境因素之一。我们之前的研究发现,热应激可诱导次生代谢产物灵芝酸(GA)的生物合成。在此,我们基于质谱进行了全面分析,以研究热应激诱导的灵芝脂质重塑。特别是,我们观察到热应激时磷脂酸(PA)显著积累。构建pld沉默菌株的进一步基因测试表明,PA的积累依赖于热应激激活的磷脂酶D(PLD)水解磷脂酰乙醇胺。此外,我们确定了PLD和PA在热应激诱导的灵芝次生代谢中的作用。外源性1-丁醇可减少PLD介导的PA形成,逆转热应激引发的灵芝酸生物合成增加。pld沉默菌株部分阻断了热应激诱导的灵芝酸生物合成,添加PA可逆转这种阻断。综上所述,我们的结果表明PLD和PA参与了热应激诱导的灵芝次生代谢调控。我们的研究结果为微生物如何应对热应激并通过磷脂重塑积累次生代谢产物提供了关键见解。

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