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转录组分析揭示了中国板栗在早期发病过程中对栗疫病菌抗性的关键基因。

Transcriptome analysis reveals key genes involved in the resistance to Cryphonectria parasitica during early disease development in Chinese chestnut.

机构信息

College of Forestry, Beijing Forestry University, Beijing, China.

College of Plant Science and Technology, Beijing University of Agriculture, Beijing, China.

出版信息

BMC Plant Biol. 2023 Feb 6;23(1):79. doi: 10.1186/s12870-023-04072-7.

DOI:10.1186/s12870-023-04072-7
PMID:36740701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9901152/
Abstract

BACKGROUND

Chestnut blight, one of the most serious branch diseases in Castanea caused by Cryphonectria parasitica, which has ravaged across American chestnut and most of European chestnut since the early twentieth century. Interestingly, the Chinese chestnut is strongly resistant to chestnut blight, shedding light on restoring the ecological status of Castanea plants severely affected by chestnut blight. To better explore the early defense of Chinese chestnut elicited in response to C. parasitica, the early stage of infection process of C. parasitica was observed and RNA sequencing-based transcriptomic profiling of responses of the chestnut blight-resistant wild resource 'HBY-1' at 0, 3 and 9 h after C. parasitica inoculation was performed.

RESULTS

First, we found that 9 h was a critical period for Chinese chestnut infected by C. parasitica, which was the basis of further study on transcriptional activation of Chinese chestnut in response to chestnut blight in the early stage. In the transcriptome analysis, a total of 283 differentially expressed genes were identified between T9 h and Mock9 h, and these DEGs were mainly divided into two clusters, one of which was metabolism-related pathways including biosynthesis of secondary metabolites, phenylpropanoid biosynthesis, amino sugar and nucleotide sugar metabolism, and photosynthesis; the other was related to plant-pathogen interaction and MAPK signal transduction. Meanwhile, the two clusters of pathways could be connected through junction among phosphatidylinositol signaling system, phytohormone signaling pathway and α-Linolenic acid metabolism pathway. It is worth noting that genes associated with JA biosynthesis and metabolic pathway were significantly up-regulated, revealing that the entire JA metabolic pathway was activated in Chinese chestnut at the early stage of chestnut blight infection.

CONCLUSION

We identified the important infection nodes of C. parasitica and observed the morphological changes of Chinese chestnut wounds at the early stage of infection. In response to chestnut blight, the plant hormone and MAPK signal transduction pathways, plant-pathogen interaction pathways and metabolism-related pathways were activated at the early stage. JA biosynthesis and metabolic pathway may be particularly involved in the Chinese chestnut resistance to chestnut blight. These results contributes to verifying the key genes involved in the resistance of Chinese chestnut to C. parasitica.

摘要

背景

栗疫病是栗属植物的一种严重枝干病害,由栗疫菌引起,自 20 世纪初以来,栗疫病已肆虐美国栗和大多数欧洲栗。有趣的是,中国板栗对栗疫病具有很强的抗性,这为恢复栗疫病严重影响的栗属植物的生态地位提供了线索。为了更好地探索中国板栗对栗疫菌早期防御机制,我们观察了栗疫菌的早期侵染过程,并对栗疫病抗性野生资源‘HBY-1’在接种栗疫菌后 0、3 和 9 h 的响应进行了基于 RNA 测序的转录组分析。

结果

首先,我们发现 9 h 是中国板栗被栗疫菌感染的关键时期,这为进一步研究中国板栗在栗疫病早期的转录激活奠定了基础。在转录组分析中,在 T9 h 和 Mock9 h 之间共鉴定到 283 个差异表达基因,这些 DEGs 主要分为两个聚类,其中一个与代谢途径相关,包括次生代谢物的生物合成、苯丙烷生物合成、氨基糖和核苷酸糖代谢以及光合作用;另一个与植物-病原菌互作和 MAPK 信号转导有关。同时,这两个途径聚类可以通过磷脂酰肌醇信号系统、植物激素信号通路和α-亚麻酸代谢通路之间的连接点连接起来。值得注意的是,与 JA 生物合成和代谢途径相关的基因显著上调,表明 JA 代谢途径在板栗感染栗疫病的早期就被激活。

结论

我们确定了栗疫菌的重要侵染节点,并观察了中国板栗伤口在感染早期的形态变化。板栗对栗疫病的反应激活了植物激素和 MAPK 信号转导途径、植物-病原菌互作途径和代谢相关途径。JA 生物合成和代谢途径可能特别参与了中国板栗对栗疫病的抗性。这些结果有助于验证中国板栗抗栗疫菌的关键基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/345fcd5ce0d5/12870_2023_4072_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/d66afb1c5033/12870_2023_4072_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/a8733dc92d06/12870_2023_4072_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/18f736d255fb/12870_2023_4072_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/e278fc3e8dad/12870_2023_4072_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/1c9f407791f8/12870_2023_4072_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/345fcd5ce0d5/12870_2023_4072_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/d66afb1c5033/12870_2023_4072_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/a8733dc92d06/12870_2023_4072_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/18f736d255fb/12870_2023_4072_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/e278fc3e8dad/12870_2023_4072_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/1c9f407791f8/12870_2023_4072_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ce/9901152/345fcd5ce0d5/12870_2023_4072_Fig6_HTML.jpg

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