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微藻宿主细胞壁与真菌碳水化合物激活酶之间的相互作用是致病寄生过程所必需的。

Interaction between the cell walls of microalgal host and fungal carbohydrate-activate enzymes is essential for the pathogenic parasitism process.

机构信息

Center for Microalgal Biotechnology and Biofuels, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, 430072, China.

State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, 430072, China.

出版信息

Environ Microbiol. 2021 Sep;23(9):5114-5130. doi: 10.1111/1462-2920.15465. Epub 2021 May 5.

Abstract

Fungi can parasitize microalgae, exerting profound impacts on both the aquatic ecosystems and microalgal mass cultures. In this study, the unicellular green alga Haematococcus pluvialis and the blastocladialean fungus Paraphysoderma sedebokerense were used as a model system to address the mechanisms underlying the fungal parasitism on the algal host. High-throughput metabolic assay indicated that P. sedebokerense can utilize several carbon sources with a preference for mannose, glucose and their oligosaccharides, which was compatible with the profile of the host algal cell walls enriched with glucan and mannan. The results of dual transcriptomics analysis suggested that P. sedebokerense can upregulate a large number of putative carbohydrate-activate enzymes (CAZymes) encoding genes, including those coding for the endo-1,4-β-glucanase and endo-1,4-β-mannanase during the infection process. The cell walls of H. pluvialis can be decomposed by both P. sedebokerense and commercial CAZymes (e.g. cellulase and endo-1,4-β-mannanase) to produce mannooligomers, while several putative parasitism-related genes of P. sedebokerense can be in turn upregulated by mannooligomers. In addition, the parasitism can be blocked by interfering the selected CAZymes including glucanase, mannanase and lysozyme with the specific inhibitors, which provided a framework for screening suitable compounds for pathogen mitigation in algal mass culture.

摘要

真菌可以寄生微藻,对水生生态系统和微藻大规模培养都有深远的影响。在这项研究中,单细胞绿藻雨生红球藻和裂殖酵母属真菌副球拟青霉被用作模型系统,以研究真菌寄生在藻类宿主上的机制。高通量代谢分析表明,副球拟青霉可以利用多种碳源,偏爱甘露糖、葡萄糖及其低聚糖,这与富含葡聚糖和甘露聚糖的宿主藻类细胞壁的特征一致。双转录组学分析的结果表明,副球拟青霉在感染过程中可以上调大量的假定碳水化合物激活酶(CAZymes)编码基因,包括内切 1,4-β-葡聚糖酶和内切 1,4-β-甘露聚糖酶。雨生红球藻的细胞壁可以被副球拟青霉和商业 CAZymes(如纤维素酶和内切 1,4-β-甘露聚糖酶)分解产生甘露寡糖,而副球拟青霉的一些假定与寄生相关的基因可以被甘露寡糖反过来上调。此外,通过用特定抑制剂干扰选定的 CAZymes(如葡聚糖酶、甘露聚糖酶和溶菌酶),可以阻止寄生,这为筛选适合藻类大规模培养中病原体缓解的合适化合物提供了框架。

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