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AozC是一种锌(II)半胱氨酸转录因子,通过控制脂肪酸生物合成负向调节米曲霉的耐盐性。

AozC, a zn(II)Cys transcription factor, negatively regulates salt tolerance in Aspergillus oryzae by controlling fatty acid biosynthesis.

作者信息

Yu Wenbin, Zhao Zeying, Zhang Yufei, Tu Yayi, He Bin

机构信息

Key Laboratory of Natural Microbial Medicine Research of Jiangxi Province, College of Life Sciences, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi, 330013, China.

出版信息

Microb Cell Fact. 2025 Jan 7;24(1):10. doi: 10.1186/s12934-024-02639-z.

DOI:10.1186/s12934-024-02639-z
PMID:39773712
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11706192/
Abstract

BACKGROUND

In the soy sauce fermentation industry, Aspergillus oryzae (A. oryzae) plays an essential role and is frequently subjected to high salinity levels, which pose a significant osmotic stress. This environmental challenge necessitates the activation of stress response mechanisms within the fungus. The Zn(II)Cys family of transcription factors, known for their zinc binuclear cluster-containing proteins, are key regulators in fungi, modulating various cellular functions such as stress adaptation and metabolic pathways.

RESULTS

Overexpression of AozC decreased growth rates in the presence of salt, while its knockdown enhanced growth, the number of spores, and biomass, particularly under conditions of 15% salt concentration, doubling these metrics compared to the wild type. Conversely, the knockdown of AozC via RNA interference significantly enhanced spore density and dry biomass, particularly under 15% salt stress, where these parameters were markedly improved over the wild type strain. Moreover, the overexpression of AozC led to a downregulation of the FAD2 gene, a pivotal enzyme in the biosynthesis of unsaturated fatty acids (UFAs), which are essential for preserving cell membrane fluidity and integrity under saline conditions. Transcriptome profiling further exposed the influence of AozC on the regulation of UFA biosynthesis and the modulation of critical stress response pathways. Notably, the regulatory role of AozC in the mitogen-activated protein kinase (MAPK) signaling and ABC transporters pathways was highlighted, underscoring its significance in cellular osmotic balance and endoplasmic reticulum homeostasis. These findings collectively indicate that AozC functions as a negative regulator of salt tolerance in A. oryzae.

CONCLUSION

This research suggest that AozC acts as a negative regulator in salt tolerance and modulates fatty acid biosynthesis in response to osmotic stress. These results provide insights into the regulatory mechanisms of stress adaptation in A. oryzae.

摘要

背景

在酱油发酵工业中,米曲霉发挥着至关重要的作用,且经常处于高盐环境中,这会造成显著的渗透胁迫。这种环境挑战促使真菌激活应激反应机制。锌(II)半胱氨酸家族转录因子以其含锌双核簇蛋白而闻名,是真菌中的关键调节因子,可调节各种细胞功能,如应激适应和代谢途径。

结果

在有盐的情况下,AozC的过表达降低了生长速率,而其敲低则提高了生长、孢子数量和生物量,特别是在15%盐浓度条件下,与野生型相比,这些指标增加了一倍。相反,通过RNA干扰敲低AozC显著提高了孢子密度和干生物量,特别是在15%盐胁迫下,这些参数比野生型菌株有显著改善。此外,AozC的过表达导致FAD2基因下调,FAD2基因是不饱和脂肪酸(UFA)生物合成中的关键酶,不饱和脂肪酸对于在盐条件下维持细胞膜流动性和完整性至关重要。转录组分析进一步揭示了AozC对UFA生物合成调控以及关键应激反应途径调节的影响。值得注意的是,突出了AozC在丝裂原活化蛋白激酶(MAPK)信号传导和ABC转运蛋白途径中的调节作用,强调了其在细胞渗透平衡和内质网稳态中的重要性。这些发现共同表明,AozC在米曲霉中作为耐盐性的负调节因子发挥作用。

结论

本研究表明,AozC在耐盐性中起负调节作用,并响应渗透胁迫调节脂肪酸生物合成。这些结果为米曲霉应激适应的调控机制提供了见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/2945fe17bf82/12934_2024_2639_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/108329cf9bba/12934_2024_2639_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/15f334cbba14/12934_2024_2639_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/c214c4f2eb1d/12934_2024_2639_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/105926279cd6/12934_2024_2639_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/2945fe17bf82/12934_2024_2639_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/108329cf9bba/12934_2024_2639_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/15f334cbba14/12934_2024_2639_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/c214c4f2eb1d/12934_2024_2639_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/105926279cd6/12934_2024_2639_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/262f/11706192/2945fe17bf82/12934_2024_2639_Fig5_HTML.jpg

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