香菇中受microRNA调控的温度影响的分枝病毒-真菌相互作用的新见解。

IF 3.8 2区 医学 Q2 VIROLOGY
Journal of Virology Pub Date : 2025-09-23 Epub Date: 2025-08-20 DOI:10.1128/jvi.00084-25
Chun-Xi Liu, Meng-Pei Guo, Jun-Zhuo Zhou, Yi-Jia Sun, Yin-Bing Bian, Zhang-Yi Xu
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引用次数: 0

摘要

病毒感染蘑菇的发病症状值得调查。本研究探讨了热胁迫(HS)对香菇分枝病毒HKB (LeV)与其蘑菇宿主香菇(Lentinula edodes)相互作用的影响,发现HS处理促进了LeV的复制,损害了宿主在菌丝完全生长时的耐热性。转录组学分析显示,对HS有应答的基因较少,耐高温相关基因在病毒感染时下调。宿主microRNA - milr -21被功能分析证明是L. edodes菌丝生长速率、耐热性和对atroviride木霉抗性的负调控因子,它可以被LeV感染和HS诱导。烟草瞬时表达实验和qRT-PCR证实,led-milR-21靶向一个与耐热性相关的转录因子LE01Gene01783。进一步分析表明,与色氨酸代谢、精氨酸和脯氨酸代谢、缬氨酸/亮氨酸和异亮氨酸降解、内质网蛋白质加工、脂肪酸降解和甘油脂代谢相关的基因可能在L. edodes对LeV感染和HS的反应中发挥作用。基于这些发现,我们提出了一种可能的机制来解释温度、LeV和L. edodes之间的相互作用。这项研究加深了我们对果体形成真菌如何应对病毒感染和非生物胁迫的理解,为全球变暖情景下潜在的病毒与宿主相互作用提供了见解。这是首次报道真菌miRNA被分枝病毒诱导。在香菇(Lentinula edodes)中,在热胁迫下感染LeV后,LeV复制激增,引发DCL1对LeV基因组的降解,特别是在其5'-UTR端和ORF1上游区域。DCL1和其他几个RNAi关键基因(如LeAGO8、LeRDR1、LeRDR5和LeRDR6)也可能在耐热性相关宿主microRNA (lead - milr -21)形成过程中被募集,导致其产量增加。因此,LE01Gene01783的led- milr -21依赖性沉默发生在LeV感染时,降低了热修复能力。这项研究加深了我们对子实体形成真菌如何应对病毒感染和非生物胁迫的理解,为全球变暖情景下潜在的病毒-宿主相互作用提供了见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
New insights into temperature-impacted mycovirus-fungus interactions regulated by a microRNA in Lentinula edodes.

The onset of symptoms in virus-infected mushrooms merits investigation. In this study, the influence of heat stress (HS) on the interaction between Lentinula edodes mycovirus HKB (LeV) and its mushroom host, Lentinula edodes, was explored, revealing that HS treatment facilitated LeV replication and compromised the host's thermotolerance at full growth of mycelia. Transcriptomic analysis showed that fewer genes responded to HS, and thermotolerance-related genes were downregulated when the virus infection occurred. A host microRNA, led-milR-21, proven as a negative regulator of the growth rate, thermotolerance, and resistance against Trichoderma atroviride of L. edodes mycelia by functional analyses, could be induced by both LeV infection and HS. Tobacco transient expression experiments with qRT-PCR confirmation demonstrated that led-milR-21 targeted a thermotolerance-related transcription factor LE01Gene01783. Further analysis showed that genes associated with tryptophan metabolism, arginine and proline metabolism, valine/leucine and isoleucine degradation, protein processing in the endoplasmic reticulum, fatty acid degradation, and glycerolipid metabolism may play roles in the responses of L. edodes to LeV infection and HS. Based on these findings, a putative mechanism was proposed to elucidate the interplay among temperature, LeV, and L. edodes. This study deepens our understanding of how fruit body-forming fungi respond to viral infection and abiotic stress, providing insights into potential virus-host interactions in a scenario of global warming.IMPORTANCEThis is the first report of a fungal miRNA being induced by a mycovirus. In Lentinula edodes, upon LeV infection under heat stress, LeV replication surges, triggering degradation of the LeV genome by DCL1, particularly on its 5'-UTR end and ORF1 upstream regions. DCL1 and several other RNAi key genes (such as LeAGO8, LeRDR1, LeRDR5, and LeRDR6) are also possibly recruited during the thermotolerance-related host microRNA (led-milR-21) formation, leading to its increased production. Consequently, led-milR-21-dependent silencing of LE01Gene01783 occurs upon LeV infection, diminishing the heat repair capacity. This study deepens our understanding of how fruiting body-forming fungi respond to viral infection and abiotic stress, providing insights into potential virus-host interactions in a scenario of global warming.

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来源期刊
Journal of Virology
Journal of Virology 医学-病毒学
CiteScore
10.10
自引率
7.40%
发文量
906
审稿时长
1 months
期刊介绍: Journal of Virology (JVI) explores the nature of the viruses of animals, archaea, bacteria, fungi, plants, and protozoa. We welcome papers on virion structure and assembly, viral genome replication and regulation of gene expression, genetic diversity and evolution, virus-cell interactions, cellular responses to infection, transformation and oncogenesis, gene delivery, viral pathogenesis and immunity, and vaccines and antiviral agents.
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