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野生马铃薯 Solanum commersonii 根部对青枯雷尔氏菌感染的转录组反应。

Transcriptome responses to Ralstonia solanacearum infection in the roots of the wild potato Solanum commersonii.

作者信息

Zuluaga A Paola, Solé Montserrat, Lu Haibin, Góngora-Castillo Elsa, Vaillancourt Brieanne, Coll Nuria, Buell C Robin, Valls Marc

机构信息

Genetics Department, Universitat de Barcelona and Centre for Research in Agricultural Genomics (CSIC-IRTA-UAB-UB) Edifici CRAG, Campus UAB, Bellaterra, 08193, Catalonia, Spain.

Department of Plant Biology, Michigan State University, East Lansing, MI, 48824, USA.

出版信息

BMC Genomics. 2015 Mar 26;16(1):246. doi: 10.1186/s12864-015-1460-1.

DOI:10.1186/s12864-015-1460-1
PMID:25880642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4391584/
Abstract

BACKGROUND

Solanum commersonii is a wild potato species that exhibits high tolerance to both biotic and abiotic stresses and has been used as a source of genes for introgression into cultivated potato. Among the interesting features of S. commersonii is resistance to the bacterial wilt caused by Ralstonia solanacearum, one of the most devastating bacterial diseases of crops.

RESULTS

In this study, we used deep sequencing of S. commersonii RNA (RNA-seq) to analyze the below-ground plant transcriptional responses to R. solanacearum. While a majority of S. commersonii RNA-seq reads could be aligned to the Solanum tuberosum Group Phureja DM reference genome sequence, we identified 2,978 S. commersonii novel transcripts through assembly of unaligned S. commersonii RNA-seq reads. We also used RNA-seq to study gene expression in pathogen-challenged roots of S. commersonii accessions resistant (F118) and susceptible (F97) to the pathogen. Expression profiles obtained from read mapping to the S. tuberosum reference genome and the S. commersonii novel transcripts revealed a differential response to the pathogen in the two accessions, with 221 (F118) and 644 (F97) differentially expressed genes including S. commersonii novel transcripts in the resistant and susceptible genotypes. Interestingly, 22.6% of the F118 and 12.8% of the F97 differentially expressed genes had been previously identified as responsive to biotic stresses and half of those up-regulated in both accessions had been involved in plant pathogen responses. Finally, we compared two different methods to eliminate ribosomal RNA from the plant RNA samples in order to allow dual mapping of RNAseq reads to the host and pathogen genomes and provide insights on the advantages and limitations of each technique.

CONCLUSIONS

Our work catalogues the S. commersonii transcriptome and strengthens the notion that this species encodes specific genes that are differentially expressed to respond to bacterial wilt. In addition, a high proportion of S. commersonii-specific transcripts were altered by R. solanacearum only in F118 accession, while phythormone-related genes were highly induced in F97, suggesting a markedly different response to the pathogen in the two plant accessions studied.

摘要

背景

康氏茄是一种野生马铃薯物种,对生物和非生物胁迫均表现出高度耐受性,已被用作基因来源,用于导入栽培马铃薯。康氏茄的一个有趣特征是对青枯雷尔氏菌引起的青枯病具有抗性,青枯病是作物中最具毁灭性的细菌性病害之一。

结果

在本研究中,我们利用康氏茄RNA的深度测序(RNA测序)来分析地下植物对青枯雷尔氏菌的转录反应。虽然大多数康氏茄RNA测序读数可以与马铃薯普通栽培种Phureja DM参考基因组序列比对,但我们通过组装未比对的康氏茄RNA测序读数鉴定出2978个康氏茄新转录本。我们还利用RNA测序研究了对该病原体具有抗性(F118)和易感性(F97)的康氏茄种质在受病原体侵染的根中的基因表达。从映射到马铃薯参考基因组和康氏茄新转录本的读数获得的表达谱揭示了这两个种质对病原体的差异反应,在抗性和易感基因型中有221个(F118)和644个(F97)差异表达基因,包括康氏茄新转录本。有趣的是,F118中22.6%和F97中12.8%的差异表达基因先前已被鉴定为对生物胁迫有反应,并且在两个种质中上调的那些基因中有一半参与了植物病原体反应。最后,我们比较了两种不同的方法来从植物RNA样本中去除核糖体RNA,以便使RNA测序读数能够双重映射到宿主和病原体基因组,并对每种技术的优缺点提供见解。

结论

我们的工作编目了康氏茄转录组,并强化了这一观点,即该物种编码特定基因,这些基因在应对青枯病时差异表达。此外,仅在F118种质中,大量康氏茄特异性转录本被青枯雷尔氏菌改变,而激素相关基因在F97中被高度诱导,这表明在所研究的两个植物种质中对病原体的反应明显不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/fdbb23551ac7/12864_2015_1460_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/345795c55940/12864_2015_1460_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/41be9ceca8a0/12864_2015_1460_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/32eb571e7fe2/12864_2015_1460_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/e0e00b2d1f70/12864_2015_1460_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/1e2ba16a7951/12864_2015_1460_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/3b86bf5b9a7e/12864_2015_1460_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/fdbb23551ac7/12864_2015_1460_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/345795c55940/12864_2015_1460_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/41be9ceca8a0/12864_2015_1460_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/32eb571e7fe2/12864_2015_1460_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/e0e00b2d1f70/12864_2015_1460_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/1e2ba16a7951/12864_2015_1460_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/3b86bf5b9a7e/12864_2015_1460_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/709a/4391584/fdbb23551ac7/12864_2015_1460_Fig7_HTML.jpg

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