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通过比较转录组学揭示大豆近等基因系对病原菌大豆疫霉的分子反应。

Molecular response to the pathogen Phytophthora sojae among ten soybean near isogenic lines revealed by comparative transcriptomics.

机构信息

Department of Agronomy, Purdue University, West Lafayette, IN 47907, USA.

出版信息

BMC Genomics. 2014 Jan 10;15:18. doi: 10.1186/1471-2164-15-18.

DOI:10.1186/1471-2164-15-18
PMID:24410936
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3893405/
Abstract

BACKGROUND

Phytophthora root and stem rot (PRR) of soybean, caused by Phytophthora sojae, is controlled by Rps genes. However, little is known regarding the Rps-induced molecular responses to P. sojae and how they actually overlap. We thus sequenced, analyzed, and compared the transcriptomes of 10 near isogenic lines (NILs), each with a unique Rps gene/allele, and the susceptible parent Williams, pre- and post-inoculation with the pathogen.

RESULTS

A total of 4,330 differentially expressed genes (DEGs) were identified in Williams versus 2,014 to 5,499 DEGs in individual NILs upon inoculation with the pathogen. Comparisons of the DEGs between the NILs and Williams identified incompatible interaction genes (IIGs) and compatible interaction genes (CIGs). Hierarchical cluster and heatmap analyses consistently grouped the NILs into three clusters: Cluster I (Rps1-a), Cluster II (Rps1-b, 1-c and 1-k) and Cluster III (Rps3-a, 3-b, 3-c, 4, 5, and 6), suggesting an overlap in Rps-induced defense signaling among certain NILs. Gene ontology (GO) analysis revealed associations between members of the WRKY family and incompatible reactions and between a number of phytohormone signaling pathways and incompatible/compatible interactions. These associations appear to be distinguished according to the NIL clusters.

CONCLUSIONS

This study characterized genes and multiple branches of putative regulatory networks associated with resistance to P. sojae in ten soybean NILs, and depicted functional "fingerprints" of individual Rps-mediated resistance responses through comparative transcriptomic analysis. Of particular interest are dramatic variations of detected DEGs, putatively involved in ethylene (ET)-, jasmonic acid (JA)-, (reactive oxygen species) ROS-, and (MAP-kinase) MAPK- signaling, among these soybean NILs, implicating their important roles of these signaling in differentiating molecular defense responses. We hypothesize that different timing and robustness in defense signaling to the same pathogen may be largely responsible for such variations.

摘要

背景

大豆疫霉根腐和茎腐病(PRR)由大豆疫霉(Phytophthora sojae)引起,可通过 Rps 基因进行控制。然而,对于 Rps 诱导的对 P. sojae 的分子响应以及它们实际上如何重叠,人们知之甚少。因此,我们对 10 个近等基因系(NIL)的转录组进行了测序、分析和比较,每个 NIL 都具有独特的 Rps 基因/等位基因,以及易感亲本威廉姆斯(Williams),在接种病原体前后。

结果

在与病原体接种后,威廉姆斯与 2014 至 5499 个差异表达基因(DEG)相比,每个 NIL 中有 4330 个差异表达基因(DEG)。比较 NIL 和威廉姆斯之间的 DEG 确定了不亲和相互作用基因(IIG)和亲和相互作用基因(CIG)。层次聚类和热图分析一致地将 NIL 分为三个聚类:聚类 I(Rps1-a)、聚类 II(Rps1-b、1-c 和 1-k)和聚类 III(Rps3-a、3-b、3-c、4、5 和 6),这表明某些 NIL 之间的 Rps 诱导防御信号存在重叠。基因本体(GO)分析显示 WRKY 家族成员与不亲和反应之间以及许多植物激素信号通路与不亲和/亲和相互作用之间存在关联。这些关联似乎根据 NIL 聚类而有所区分。

结论

本研究描述了十个大豆 NIL 中与 P. sojae 抗性相关的基因和多个假定调控网络分支,并通过比较转录组分析描绘了单个 Rps 介导的抗性反应的功能“指纹”。特别有趣的是,在这些大豆 NIL 中,与乙烯(ET)、茉莉酸(JA)、(活性氧物种)ROS 和(MAP 激酶)MAPK 信号相关的检测到的 DEG 存在明显变化,暗示它们在区分分子防御反应中的重要作用。我们假设,对同一病原体的防御信号的不同时间和稳健性可能在很大程度上导致了这种变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/cb63af20aaf6/1471-2164-15-18-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/93f8a72bea25/1471-2164-15-18-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/1d61743db788/1471-2164-15-18-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/2cd3303cb422/1471-2164-15-18-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/3a75908623f3/1471-2164-15-18-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/8de835f2d7c4/1471-2164-15-18-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/cb63af20aaf6/1471-2164-15-18-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/93f8a72bea25/1471-2164-15-18-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/1d61743db788/1471-2164-15-18-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/2cd3303cb422/1471-2164-15-18-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0917/3893405/3a75908623f3/1471-2164-15-18-4.jpg
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