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一氧化氮介导的几丁质酶活性调控及镉螯合在拟南芥对镉胁迫响应中的作用

Nitric Oxide-Mediated Regulation of Chitinase Activity and Cadmium Sequestration in the Response of to Cadmium Stress.

作者信息

Li Dongxu, Chu Chen, Zhao Mengshi, Hou Suying, Ji Rong, Liu Changhong

机构信息

State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210023, China.

College of Life Sciences, Yunnan University, Kunming 650500, China.

出版信息

Microorganisms. 2025 Feb 20;13(3):470. doi: 10.3390/microorganisms13030470.

DOI:10.3390/microorganisms13030470
PMID:40142363
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11944285/
Abstract

is an edible fungus with high medicinal value, but exposure to heavy-metal pollution poses significant health risks. Cadmium (Cd) toxicity inhibits fungal growth and leads to Cd accumulation in the mycelium. However, the regulatory mechanisms of Cd-induced growth inhibition and Cd accumulation remain poorly understood. Here, 20R-7-F01 was cultured in Cd-supplemented minimal medium (MM) to investigate the response of 20R-7-F01 to Cd exposure. We found that Cd exposure resulted in growth inhibition and a Cd-dependent increase in endogenous nitric oxide (NO) levels. NO production was primarily mediated by the nitrate reductase (NR) pathway. Cd-induced growth inhibition was alleviated by inhibiting NR activity or scavenging NO, highlighting the role of NO in stress responses. Furthermore, NO was found to enhance chitinase activity, thereby promoting Cd accumulation in the fungal cell wall and leading to growth inhibition. These results reveal a novel mechanism by which copes with Cd stress. This study highlights the potential of manipulating NO levels as a strategy to enhance fungal tolerance to heavy-metal pollution, providing a new avenue for managing environmental stresses in edible fungi and protecting human health.

摘要

是一种具有高药用价值的食用菌,但暴露于重金属污染会带来重大健康风险。镉(Cd)毒性会抑制真菌生长并导致菌丝体中镉的积累。然而,镉诱导生长抑制和镉积累的调控机制仍知之甚少。在此,将20R - 7 - F01在添加镉的基本培养基(MM)中培养,以研究20R - 7 - F01对镉暴露的反应。我们发现镉暴露导致生长抑制以及内源性一氧化氮(NO)水平的镉依赖性增加。NO的产生主要由硝酸还原酶(NR)途径介导。通过抑制NR活性或清除NO可缓解镉诱导的生长抑制,突出了NO在应激反应中的作用。此外,发现NO会增强几丁质酶活性,从而促进镉在真菌细胞壁中的积累并导致生长抑制。这些结果揭示了应对镉胁迫的一种新机制。本研究突出了调控NO水平作为增强真菌对重金属污染耐受性策略的潜力,为管理食用菌中的环境胁迫和保护人类健康提供了一条新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/f2e81f9d4334/microorganisms-13-00470-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/765d2002322d/microorganisms-13-00470-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/563271529bfa/microorganisms-13-00470-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/396d64514b81/microorganisms-13-00470-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/c1c8e2aec422/microorganisms-13-00470-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/300d12162c57/microorganisms-13-00470-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/d1de576e6788/microorganisms-13-00470-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/f2e81f9d4334/microorganisms-13-00470-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/765d2002322d/microorganisms-13-00470-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/563271529bfa/microorganisms-13-00470-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/396d64514b81/microorganisms-13-00470-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/c1c8e2aec422/microorganisms-13-00470-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/300d12162c57/microorganisms-13-00470-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/d1de576e6788/microorganisms-13-00470-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f33/11944285/f2e81f9d4334/microorganisms-13-00470-g007.jpg

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