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

Identifieur interne : 001773 ( Main/Exploration ); précédent : 001772; suivant : 001774

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 : pubmed:26768277

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.


DOI: 10.1186/s12864-015-2286-6
PubMed: 26768277
PubMed Central: PMC4714501


Affiliations:


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<term>Basidiomycota (genetics)</term>
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<term>Disease Resistance (genetics)</term>
<term>Gene Expression Regulation, Plant (genetics)</term>
<term>Host-Pathogen Interactions (genetics)</term>
<term>MicroRNAs (genetics)</term>
<term>Plant Diseases (genetics)</term>
<term>Plant Diseases (microbiology)</term>
<term>Plant Immunity (genetics)</term>
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<term>Basidiomycota (génétique)</term>
<term>Basidiomycota (pathogénicité)</term>
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<term>Feuilles de plante (microbiologie)</term>
<term>Immunité des plantes (génétique)</term>
<term>Interactions hôte-pathogène (génétique)</term>
<term>Maladies des plantes (génétique)</term>
<term>Maladies des plantes (microbiologie)</term>
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<term>Populus (microbiologie)</term>
<term>Régulation de l'expression des gènes végétaux (génétique)</term>
<term>Résistance à la maladie (génétique)</term>
<term>Transduction du signal (génétique)</term>
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<term>Basidiomycota</term>
<term>Disease Resistance</term>
<term>Gene Expression Regulation, Plant</term>
<term>Host-Pathogen Interactions</term>
<term>Plant Diseases</term>
<term>Plant Immunity</term>
<term>Plant Leaves</term>
<term>Populus</term>
<term>Signal Transduction</term>
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<term>Basidiomycota</term>
<term>Feuilles de plante</term>
<term>Immunité des plantes</term>
<term>Interactions hôte-pathogène</term>
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<term>Régulation de l'expression des gènes végétaux</term>
<term>Résistance à la maladie</term>
<term>Transduction du signal</term>
<term>microARN</term>
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<p>
<b>BACKGROUND</b>
</p>
<p>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).</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>RESULTS</b>
</p>
<p>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.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>CONCLUSIONS</b>
</p>
<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>
</div>
</front>
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<Year>2016</Year>
<Month>09</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised>
<Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
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<Day>15</Day>
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<Title>BMC genomics</Title>
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<Abstract>
<AbstractText Label="BACKGROUND" NlmCategory="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).</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="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.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="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.</AbstractText>
</Abstract>
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<LastName>Li</LastName>
<ForeName>Danlei</ForeName>
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<Affiliation>College of Forestry, Northeast Forestry University, Harbin, 150040, China. danleili@126.com.</Affiliation>
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<LastName>Wang</LastName>
<ForeName>Feng</ForeName>
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<Affiliation>College of Forestry, Northeast Forestry University, Harbin, 150040, China. kingsummit@126.com.</Affiliation>
</AffiliationInfo>
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<LastName>Wang</LastName>
<ForeName>Chao</ForeName>
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<Affiliation>College of Forestry, Northeast Forestry University, Harbin, 150040, China. plantdisease@126.com.</Affiliation>
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<LastName>Zou</LastName>
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<Affiliation>College of Forestry, Northeast Forestry University, Harbin, 150040, China. rustfungi@163.com.</Affiliation>
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<LastName>Wang</LastName>
<ForeName>Zhiying</ForeName>
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<Affiliation>College of Forestry, Northeast Forestry University, Harbin, 150040, China. nematodefungi@126.com.</Affiliation>
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<Author ValidYN="Y">
<LastName>Chen</LastName>
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