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真菌特异性转录因子VpFSTF1是[具体物种]致病力所必需的。 (注:原文中“in.”后面内容缺失,根据已有信息补充完整,实际翻译时需根据完整内容准确翻译)

The Fungal-Specific Transcription Factor VpFSTF1 Is Required for Virulence in .

作者信息

Kange Alex Machio, Xia Ai, Si Jierui, Li Bingxin, Zhang Xiong, Ai Gan, He Feng, Dou Daolong

机构信息

Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, Nanjing, China.

School of Life Sciences, Anhui Normal University, Wuhu, China.

出版信息

Front Microbiol. 2020 Jan 10;10:2945. doi: 10.3389/fmicb.2019.02945. eCollection 2019.

DOI:10.3389/fmicb.2019.02945
PMID:31998257
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6965324/
Abstract

is the causal agent of pear canker disease, which leads to enormous losses of pear production in eastern Asian, especially China. In this study, we identified a fungal-specific transcription factor 1 (termed as VpFSTF1) from , which is highly conserved in fungi. To characterize its functions, we generated mutant and complementation strains in and found that mutants lost the ability to form fruiting bodies along with the reduced virulence. The radial growth of mutant was sensitive to increasing concentrations of hydrogen peroxide (HO) and salicylic acid (SA). Moreover, RNA-sequencing (RNA-Seq) analysis of wild-type (WT) and mutant strains was performed, and the results revealed 1,993 upregulated, and 2006 downregulated differentially expressed genes (DEGs) in the mutant. The DEGs were corresponding to the genes that are involved in amino acid metabolism, starch, and sucrose metabolism, gluconeogenesis, citrate cycle, and carbon metabolism. Interestingly, pathogen host interaction (PHI) analysis showed that 69 downregulated genes were related to virulence, suggesting that they might function downstream of VpFSTF1. Nine DEGs were further validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and the results were consistent with RNA-seq analysis. Furthermore, promoter regions were predicted, and VpFSTF1 binding activity was assessed. We demonstrated that five promoters are directly or indirectly targeted by VpFSTF1, including catalase-related peroxidase (VPIG_01209) and P450 family genes. Taken together, these findings indicate that VpFSTF1 is crucial for the virulence of via direct or indirect regulation of downstream genes expression and lay an important foundation for understanding the molecular mechanism of infection.

摘要

是梨溃疡病的致病因子,该病在东亚尤其是中国导致梨产量的巨大损失。在本研究中,我们从 中鉴定出一种真菌特异性转录因子1(称为VpFSTF1),它在真菌中高度保守。为了表征其功能,我们在 中构建了突变体和互补菌株,发现 突变体失去了形成子实体的能力,同时毒力降低。 突变体的径向生长对过氧化氢(HO)和水杨酸(SA)浓度的增加敏感。此外,对野生型(WT)和 突变体菌株进行了RNA测序(RNA-Seq)分析,结果显示突变体中有1993个上调和2006个下调的差异表达基因(DEG)。这些DEG与参与氨基酸代谢、淀粉和蔗糖代谢、糖异生、柠檬酸循环和碳代谢的基因相对应。有趣的是,病原体-宿主相互作用(PHI)分析表明,69个下调基因与毒力相关,表明它们可能在VpFSTF1的下游发挥作用。通过定量逆转录-聚合酶链反应(qRT-PCR)进一步验证了9个DEG,结果与RNA-seq分析一致。此外,预测了启动子区域,并评估了VpFSTF1的结合活性。我们证明了五个启动子直接或间接被VpFSTF1靶向,包括过氧化氢酶相关过氧化物酶(VPIG_01209)和细胞色素P450家族基因。综上所述,这些发现表明VpFSTF1通过直接或间接调节下游基因表达对 的毒力至关重要,为理解 感染的分子机制奠定了重要基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/d01ae742800b/fmicb-10-02945-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/9ecf901d8dc4/fmicb-10-02945-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/3a55842f39b7/fmicb-10-02945-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/d97e88855c2b/fmicb-10-02945-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/427b48b4504c/fmicb-10-02945-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/77261ea3e397/fmicb-10-02945-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/1da5c45bd95e/fmicb-10-02945-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/c65680f66563/fmicb-10-02945-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/22211a7a66a4/fmicb-10-02945-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/d01ae742800b/fmicb-10-02945-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/9ecf901d8dc4/fmicb-10-02945-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/3a55842f39b7/fmicb-10-02945-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/d97e88855c2b/fmicb-10-02945-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/427b48b4504c/fmicb-10-02945-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/77261ea3e397/fmicb-10-02945-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/1da5c45bd95e/fmicb-10-02945-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/c65680f66563/fmicb-10-02945-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/22211a7a66a4/fmicb-10-02945-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b15d/6965324/d01ae742800b/fmicb-10-02945-g009.jpg

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