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植物病原物隔孢腔菌属物种的比较基因组学和病原菌感染过程中的胶孢炭疽菌转录组学研究揭示了该属的致病策略。

Comparative genomics of plant pathogenic Diaporthe species and transcriptomics of Diaporthe caulivora during host infection reveal insights into pathogenic strategies of the genus.

机构信息

Departamento de Biología Molecular, Instituto de Investigaciones Biológicas Clemente Estable, Avenida Italia 3318, CP 11600, Montevideo, Uruguay.

Instituto Nacional de Investigación Agropecuaria (INIA), Estación Experimental INIA Las Brujas, Ruta 48 Km 10, Canelones, Uruguay.

出版信息

BMC Genomics. 2022 Mar 3;23(1):175. doi: 10.1186/s12864-022-08413-y.

DOI:10.1186/s12864-022-08413-y
PMID:35240994
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8896106/
Abstract

BACKGROUND

Diaporthe caulivora is a fungal pathogen causing stem canker in soybean worldwide. The generation of genomic and transcriptomic information of this ascomycete, together with a comparative genomic approach with other pathogens of this genus, will contribute to get insights into the molecular basis of pathogenicity strategies used by D. caulivora and other Diaporthe species.

RESULTS

In the present work, the nuclear genome of D. caulivora isolate (D57) was resolved, and a comprehensive annotation based on gene expression and genomic analysis is provided. Diaporthe caulivora D57 has an estimated size of 57,86 Mb and contains 18,385 predicted protein-coding genes, from which 1501 encode predicted secreted proteins. A large array of D. caulivora genes encoding secreted pathogenicity-related proteins was identified, including carbohydrate-active enzymes (CAZymes), necrosis-inducing proteins, oxidoreductases, proteases and effector candidates. Comparative genomics with other plant pathogenic Diaporthe species revealed a core secretome present in all Diaporthe species as well as Diaporthe-specific and D. caulivora-specific secreted proteins. Transcriptional profiling during early soybean infection stages showed differential expression of 2659 D. caulivora genes. Expression patterns of upregulated genes and gene ontology enrichment analysis revealed that host infection strategies depends on plant cell wall degradation and modification, detoxification of compounds, transporter activities and toxin production. Increased expression of effectors candidates suggests that D. caulivora pathogenicity also rely on plant defense evasion. A high proportion of the upregulated genes correspond to the core secretome and are represented in the pathogen-host interaction (PHI) database, which is consistent with their potential roles in pathogenic strategies of the genus Diaporthe.

CONCLUSIONS

Our findings give novel and relevant insights into the molecular traits involved in pathogenicity of D. caulivora towards soybean plants. Some of these traits are in common with other Diaporthe pathogens with different host specificity, while others are species-specific. Our analyses also highlight the importance to have a deeper understanding of pathogenicity functions among Diaporthe pathogens and their interference with plant defense activation.

摘要

背景

Diaporthe caulivora 是一种真菌病原体,可导致全球大豆的茎溃疡。该子囊菌的基因组和转录组信息的产生,以及与该属其他病原体的比较基因组方法,将有助于深入了解 D. caulivora 和其他 Diaporthe 物种致病策略的分子基础。

结果

本工作解析了 D. caulivora 分离株(D57)的核基因组,并基于基因表达和基因组分析提供了全面的注释。D. caulivora D57 的估计大小为 57.86 Mb,包含 18385 个预测的蛋白编码基因,其中 1501 个编码预测的分泌蛋白。鉴定了大量编码分泌致病性相关蛋白的 D. caulivora 基因,包括碳水化合物活性酶(CAZymes)、坏死诱导蛋白、氧化还原酶、蛋白酶和效应子候选物。与其他植物病原性 Diaporthe 物种的比较基因组学揭示了所有 Diaporthe 物种以及 Diaporthe 特异性和 D. caulivora 特异性分泌蛋白中存在的核心分泌组。在早期大豆感染阶段的转录谱分析显示,2659 个 D. caulivora 基因的表达差异。上调基因的表达模式和基因本体富集分析表明,宿主感染策略依赖于植物细胞壁的降解和修饰、化合物的解毒、转运蛋白的活性和毒素的产生。效应子候选物的高表达表明 D. caulivora 的致病性也依赖于植物防御逃避。上调基因的很大一部分对应于核心分泌组,并在病原体-宿主相互作用(PHI)数据库中表示,这与其在 Diaporthe 属致病策略中的潜在作用一致。

结论

我们的研究结果为 D. caulivora 对大豆植物致病性相关的分子特征提供了新的和相关的见解。这些特征中的一些与其他具有不同宿主特异性的 Diaporthe 病原体共有,而另一些则是物种特异性的。我们的分析还强调了深入了解 Diaporthe 病原体的致病性功能及其对植物防御激活的干扰的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/7fb87868e504/12864_2022_8413_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/bbd046afa02f/12864_2022_8413_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/9eba6ce081b6/12864_2022_8413_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/100210863b64/12864_2022_8413_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/7fb87868e504/12864_2022_8413_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/bbd046afa02f/12864_2022_8413_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/0ad5d9ba6eca/12864_2022_8413_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/246cfcb826d5/12864_2022_8413_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/9eba6ce081b6/12864_2022_8413_Fig4_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8de9/8896106/7fb87868e504/12864_2022_8413_Fig6_HTML.jpg

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