Hubei Key Laboratory of Industrial Microbiology, Hubei Provincial Cooperative Innovation Center of Industrial Fermentation, Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei University of Technology, Wuhan, China.
Hubei Key Laboratory of Industrial Microbiology, Hubei Provincial Cooperative Innovation Center of Industrial Fermentation, Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei University of Technology, Wuhan, China
Appl Environ Microbiol. 2018 Oct 30;84(22). doi: 10.1128/AEM.01840-18. Print 2018 Nov 15.
Adaptation to environmental perturbations requires living systems to coordinately regulate signaling pathways, gene expression, and metabolism. To better understand the mechanisms underlying adaptation, the regulatory nodes within networks must be elucidated. Here, (which encodes an aminotransferase), (which encodes a decarboxylase), and (which encodes a demethiolase) were identified as key genes involved in the catabolism of methionine in the mycoparasitic fungus , isolated from ascocarps. Exogenous Met induced the transcription of and but repressed the transcription of , which is controlled by the putative MSN2 and GLN3 binding sites responding to nitrogen catabolite repression. Met and its structural derivatives function as glutamine synthetase inhibitors, resulting in the downregulation of expression. The putative GLN3 binding site was necessary for downregulation. In , Met and its structural derivatives also triggered downregulation of demethiolase gene expression. Altogether, the results indicated that exogenous Met triggered nitrogen catabolite repression, which stimulated the Ehrlich pathway and negatively regulated the demethiolation pathway via the methionine sulfoximine-responsive regulatory pathway. This finding revealed the regulatory nodes within the networks controlling the catabolism of Met into volatile organic sulfur-containing compounds, thereby enhancing our understanding of adaptation. Methionine shuttles organic nitrogen and plays a central role in nitrogen metabolism. Exogenous Met strongly induces the expression of and , represses the expression of , and generates volatile organic sulfur-containing compounds via the Ehrlich and demethiolation pathways. In this study, we used genetic, bioinformatic, and metabolite-based analyses to confirm that transcriptional control of the aminotransferase gene , the decarboxylase gene , and the demethiolase gene modulates Met catabolism into volatile organic sulfur-containing compounds. Importantly, we found that, in addition to the Ehrlich pathway, the demethiolation pathway was regulated by a nitrogen catabolite repression-sensitive regulatory pathway that controlled the transcription of genes required to catabolize poor nitrogen sources. This work significantly advances our understanding of nitrogen catabolite repression-sensitive transcriptional regulation of sulfur-containing amino acid catabolism and provides a basis for engineering Met catabolism pathways for the production of fuel and valuable flavor alcohols.
适应环境干扰需要生命系统协调调控信号通路、基因表达和代谢。为了更好地理解适应的机制，必须阐明网络中的调节节点。在这里，(编码一种氨基转移酶)、(编码一种脱羧酶)和(编码一种去硫醇酶)被鉴定为参与真菌分解甲硫氨酸的关键基因，该真菌从ascocarps 中分离出来。外源性 Met 诱导基因和的转录，但抑制的转录，这是由氮分解代谢物抑制响应的假定 MSN2 和 GLN3 结合位点控制的。Met 和其结构衍生物作为谷氨酰胺合成酶抑制剂，导致表达下调。假定的 GLN3 结合位点对于下调是必要的。在中，Met 和其结构衍生物也触发了脱硫醇酶基因表达的下调。总的来说，结果表明外源性 Met 触发了氮分解代谢物抑制，这刺激了 Ehrlich 途径，并通过甲硫氨酸亚砜响应的调节途径负调控脱硫醇途径。这一发现揭示了控制 Met 分解为挥发性有机含硫化合物的网络中的调节节点，从而增强了我们对适应的理解。甲硫氨酸穿梭有机氮，在氮代谢中起核心作用。外源性 Met 强烈诱导基因和的表达，抑制的表达，并通过 Ehrlich 和脱硫醇途径产生挥发性有机含硫化合物。在这项研究中，我们使用遗传、生物信息学和基于代谢物的分析来证实，氨基转移酶基因、脱羧酶基因和脱硫醇酶基因的转录控制调节 Met 分解为挥发性有机含硫化合物。重要的是，我们发现，除了 Ehrlich 途径外，脱硫醇途径还受到氮分解代谢物抑制敏感调节途径的调节，该途径控制分解不良氮源所需基因的转录。这项工作显著推进了我们对含硫氨基酸代谢的氮分解代谢物抑制敏感转录调控的理解，并为工程 Met 代谢途径生产燃料和有价值的风味醇提供了基础。
