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MicroRNA-mediated susceptible poplar gene expression regulation associated with the infection of virulent Melampsora larici-populina

Identifieur interne : 000624 ( Main/Exploration ); précédent : 000623; suivant : 000625

MicroRNA-mediated susceptible poplar gene expression regulation associated with the infection of virulent Melampsora larici-populina

Auteurs : Danlei Li [République populaire de Chine] ; Feng Wang [République populaire de Chine] ; Chao Wang [République populaire de Chine] ; Li Zou [République populaire de Chine] ; Zhiying Wang [République populaire de Chine] ; Qiaoli Chen [République populaire de Chine] ; Chunyang Niu [République populaire de Chine] ; Ruizhi Zhang [République populaire de Chine] ; Yaming Ling [République populaire de Chine] ; Bowen Wang [République populaire de Chine]

Source :

RBID : PMC:4714501

Descripteurs français

English descriptors

Abstract

Background

Rust caused by Melampsora larici-populina is one of the most damaging diseases of poplars. Rust is considered to be a model pathogen for genetic studies because both pathogen and host genomes are available. The poplar ‘Robusta’, whose general rust resistance is defeated by virulent rust E4, provides suitable host material for studies of the gene regulation involved in rust resistance/susceptibility. In this study, we investigated the microRNA-mediated susceptible poplar gene expression regulation associated with the infection of virulent rust. We were particularly interested in delineating the host-pathogen interactions with a specific focus on microRNAs (miRNAs).

Results

To study the susceptibility of poplar to M. larici-populina, small RNA (sRNA) libraries, a degradome cDNA library and digital gene expression libraries were constructed for rust-inoculated and rust-free susceptible poplar ‘Robusta’ leaves through high-throughput sequencing. Altogether, 12,722 regulating interactions were identified. The results delineated the framework of post-transcriptional regulation of gene expression in the susceptible poplar, which was infected by the virulent rust. The results indicated that pathogen-associated molecular patterns (PAMPs) and PAMP-triggered immunity were induced by the infection of virulent rust E4 and that miRNAs still functioned at this stage. After this stage, miRNA-regulated R genes, such as TIR-NBS-LRR and CC-NBS-LRR, were not fully functional. Additionally, the rust-responsive miRNAs did not regulate the signaling component genes related to the salicylic acid pathway or the hypersensitive response.

Conclusions

We found that the defense-related post-transcriptional regulation of the susceptible poplar ‘Robusta’ functions normally only at the stage of PAMPs and PAMP-triggered immunity (PTI). More importantly, the miRNA-mediated post-transcriptional regulation of defense signal pathway genes were inactivated by the infection of virulent rust at the stage of effector-triggered susceptibility and during the following stages of salicylic acid and hypersensitive responses. This inactivation was the major characteristic of ‘Robusta’ susceptibility.

Electronic supplementary material

The online version of this article (doi:10.1186/s12864-015-2286-6) contains supplementary material, which is available to authorized users.


Url:
DOI: 10.1186/s12864-015-2286-6
PubMed: 26768277
PubMed Central: 4714501


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

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<term>Host-Pathogen Interactions (genetics)</term>
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<term>Feuilles de plante (microbiologie)</term>
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<term>Populus (microbiologie)</term>
<term>Régulation de l'expression des gènes végétaux (génétique)</term>
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<term>Transduction du signal (génétique)</term>
<term>microARN (génétique)</term>
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<term>Plant Leaves</term>
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<term>Signal Transduction</term>
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<term>Interactions hôte-pathogène</term>
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<term>microARN</term>
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<div type="abstract" xml:lang="en">
<sec>
<title>Background</title>
<p>Rust caused by
<italic>Melampsora larici-populina</italic>
is one of the most damaging diseases of poplars. Rust is considered to be a model pathogen for genetic studies because both pathogen and host genomes are available. The poplar ‘Robusta’, whose general rust resistance is defeated by virulent rust E4, provides suitable host material for studies of the gene regulation involved in rust resistance/susceptibility. In this study, we investigated the microRNA-mediated susceptible poplar gene expression regulation associated with the infection of virulent rust. We were particularly interested in delineating the host-pathogen interactions with a specific focus on microRNAs (miRNAs).</p>
</sec>
<sec>
<title>Results</title>
<p>To study the susceptibility of poplar to
<italic>M. larici-populina</italic>
, small RNA (sRNA) libraries, a degradome cDNA library and digital gene expression libraries were constructed for rust-inoculated and rust-free susceptible poplar ‘Robusta’ leaves through high-throughput sequencing. Altogether, 12,722 regulating interactions were identified. The results delineated the framework of post-transcriptional regulation of gene expression in the susceptible poplar, which was infected by the virulent rust. The results indicated that pathogen-associated molecular patterns (PAMPs) and PAMP-triggered immunity were induced by the infection of virulent rust E4 and that miRNAs still functioned at this stage. After this stage, miRNA-regulated
<italic>R</italic>
genes, such as TIR-NBS-LRR and CC-NBS-LRR, were not fully functional. Additionally, the rust-responsive miRNAs did not regulate the signaling component genes related to the salicylic acid pathway or the hypersensitive response.</p>
</sec>
<sec>
<title>Conclusions</title>
<p>We found that the defense-related post-transcriptional regulation of the susceptible poplar ‘Robusta’ functions normally only at the stage of PAMPs and PAMP-triggered immunity (PTI). More importantly, the miRNA-mediated post-transcriptional regulation of defense signal pathway genes were inactivated by the infection of virulent rust at the stage of effector-triggered susceptibility and during the following stages of salicylic acid and hypersensitive responses. This inactivation was the major characteristic of ‘Robusta’ susceptibility.</p>
</sec>
<sec>
<title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1186/s12864-015-2286-6) contains supplementary material, which is available to authorized users.</p>
</sec>
</div>
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