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向致病生活方式进化的丛梗孢 PR-1 蛋白的适应性进化。

Adaptive evolution of Moniliophthora PR-1 proteins towards its pathogenic lifestyle.

机构信息

Departamento de Genética, Evolução, Microbiologia e Imunologia, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, SP, Brazil.

Departamento de Ciências Biológicas, Escola Superior de Agricultura "Luiz de Queiroz" (ESALQ), Universidade de São Paulo, Piracicaba, SP, Brazil.

出版信息

BMC Ecol Evol. 2021 May 14;21(1):84. doi: 10.1186/s12862-021-01818-5.

DOI:10.1186/s12862-021-01818-5
PMID:33990179
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8120714/
Abstract

BACKGROUND

Plant pathogenesis related-1 (PR-1) proteins belong to the CAP superfamily and have been characterized as markers of induced defense against pathogens. Moniliophthora perniciosa and Moniliophthora roreri are hemibiotrophic fungi that respectively cause the witches' broom disease and frosty pod rot in Theobroma cacao. Interestingly, a large number of plant PR-1-like genes are present in the genomes of both species and many are up-regulated during the biotrophic interaction. In this study, we investigated the evolution of PR-1 proteins from 22 genomes of Moniliophthora isolates and 16 other Agaricales species, performing genomic investigation, phylogenetic reconstruction, positive selection search and gene expression analysis.

RESULTS

Phylogenetic analysis revealed conserved PR-1 genes (PR-1a, b, d, j), shared by many Agaricales saprotrophic species, that have diversified in new PR-1 genes putatively related to pathogenicity in Moniliophthora (PR-1f, g, h, i), as well as in recent specialization cases within M. perniciosa biotypes (PR-1c, k, l) and M. roreri (PR-1n). PR-1 families in Moniliophthora with higher evolutionary rates exhibit induced expression in the biotrophic interaction and positive selection clues, supporting the hypothesis that these proteins accumulated adaptive changes in response to host-pathogen arms race. Furthermore, although previous work showed that MpPR-1 can detoxify plant antifungal compounds in yeast, we found that in the presence of eugenol M. perniciosa differentially expresses only MpPR-1e, k, d, of which two are not linked to pathogenicity, suggesting that detoxification might not be the main function of most MpPR-1.

CONCLUSIONS

Based on analyses of genomic and expression data, we provided evidence that the evolution of PR-1 in Moniliophthora was adaptive and potentially related to the emergence of the parasitic lifestyle in this genus. Additionally, we also discuss how fungal PR-1 proteins could have adapted from basal conserved functions to possible roles in fungal pathogenesis.

摘要

背景

植物病程相关 1（PR-1）蛋白属于 CAP 超家族，被认为是对病原体诱导防御的标志物。Moniliophthora perniciosa 和 Moniliophthora roreri 是半活体真菌，分别导致可可树的女巫扫帚病和霜霉病。有趣的是，这两个物种的基因组中都存在大量的植物 PR-1 样基因，其中许多在生物互作过程中上调。在这项研究中，我们调查了来自 22 个 Moniliophthora 分离株和 16 个其他 Agaricales 物种的 PR-1 蛋白的进化，进行了基因组研究、系统发育重建、正选择搜索和基因表达分析。

结果

系统发育分析显示，保守的 PR-1 基因（PR-1a、b、d、j）存在于许多 Agaricales 腐生种中，它们在 Moniliophthora 中与致病性相关的新 PR-1 基因（PR-1f、g、h、i）中多样化，以及在 M. perniciosa 生物型（PR-1c、k、l）和 M. roreri（PR-1n）的近期特化案例中多样化。Moniliophthora 中进化速率较高的 PR-1 家族在生物互作中表现出诱导表达和正选择线索，支持这些蛋白在应对宿主-病原体军备竞赛中积累适应性变化的假说。此外，尽管之前的工作表明 MpPR-1 可以在酵母中解毒植物抗真菌化合物，但我们发现，在丁香酚存在的情况下，M. perniciosa 仅差异表达 MpPR-1e、k、d，其中两个与致病性无关，这表明解毒可能不是大多数 MpPR-1 的主要功能。

结论

基于基因组和表达数据的分析，我们提供了证据表明 Moniliophthora 中 PR-1 的进化是适应性的，可能与该属寄生生活方式的出现有关。此外，我们还讨论了真菌 PR-1 蛋白如何从基础保守功能适应到真菌发病机制中的可能作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/4ee87c0387c9/12862_2021_1818_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/ac57a1c9a9d5/12862_2021_1818_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/aaaff636ec6b/12862_2021_1818_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/2f197f72fe89/12862_2021_1818_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/c7e78323d4cc/12862_2021_1818_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/1c696e7d4d12/12862_2021_1818_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/4ee87c0387c9/12862_2021_1818_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/ac57a1c9a9d5/12862_2021_1818_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/aaaff636ec6b/12862_2021_1818_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/2f197f72fe89/12862_2021_1818_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/c7e78323d4cc/12862_2021_1818_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/1c696e7d4d12/12862_2021_1818_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1071/8120714/4ee87c0387c9/12862_2021_1818_Fig6_HTML.jpg

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