Serveur d'exploration sur les effecteurs de phytopathogènes

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Nbnrp1 Mediates Verticillium dahliae Effector PevD1-Triggered Defense Responses by Regulating Sesquiterpenoid Phytoalexins Biosynthesis Pathway in Nicotiana benthamiana.

Identifieur interne : 000100 ( Main/Exploration ); précédent : 000099; suivant : 000101

Nbnrp1 Mediates Verticillium dahliae Effector PevD1-Triggered Defense Responses by Regulating Sesquiterpenoid Phytoalexins Biosynthesis Pathway in Nicotiana benthamiana.

Auteurs : Yingbo Liang [République populaire de Chine] ; Ze Li [République populaire de Chine] ; Yi Zhang [République populaire de Chine] ; Fanlu Meng [République populaire de Chine] ; Dewen Qiu [République populaire de Chine] ; Hongmei Zeng [République populaire de Chine] ; Guangyue Li [République populaire de Chine] ; Xiufen Yang [République populaire de Chine]

Source :

RBID : pubmed:33186613

Abstract

PevD1, a fungal effector secreted by Verticillium dahliae, could induce hypersensitive responses-like necrosis and systemic acquired resistance (SAR) in cotton and tobacco plants. PevD1 could drastically induce the expression of Nbnrp1, which is an asparagine-rich protein (NRP) of Nicotiana benthamiana. Our previous research indicated that Nbnrp1 positively regulated PevD1-induced cell necrosis and disease resistance. In this study, we further investigated PevD1-induced immune responses in both wild-type (WT) and Nbnrp1-RNAi lines through RNA-seq, in order to reveal the underlying mechanism of Nbnrp1-modulated PevD1-induced disease resistance in N. benthamiana. Results showed that Nbnrp1-RNAi lines exhibited reduced PevD1-induced immune responses, like inhibiting H2O2 accumulation and MAPK phosphorylation. To silence Nbnrp1 inhibited the expression of PevD1-induced differential expression genes (DEGs) involved in pathways associated with sesquiterpenoid and triterpenoid biosynthesis, flavone and flavonol biosynthesis, plant-pathogen interaction and phenylpropanoid biosynthesis, etc. It is worth noting that sesquiterpene phytoalexin capsidiol accumulation were obviously decreased in Nbnrp1-RNAi plants after PevD1 treatment, accompanied with the down-expression of EAS and EAH, which were two key genes related to capsidiol biosynthesis. These results suggested that Nbnrp1 mediates PevD1-induced defense responses by regulating sesquiterpenoid phytoalexins biosynthesis pathway.

DOI: 10.1016/j.gene.2020.145280
PubMed: 33186613


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<div type="abstract" xml:lang="en">PevD1, a fungal effector secreted by Verticillium dahliae, could induce hypersensitive responses-like necrosis and systemic acquired resistance (SAR) in cotton and tobacco plants. PevD1 could drastically induce the expression of Nbnrp1, which is an asparagine-rich protein (NRP) of Nicotiana benthamiana. Our previous research indicated that Nbnrp1 positively regulated PevD1-induced cell necrosis and disease resistance. In this study, we further investigated PevD1-induced immune responses in both wild-type (WT) and Nbnrp1-RNAi lines through RNA-seq, in order to reveal the underlying mechanism of Nbnrp1-modulated PevD1-induced disease resistance in N. benthamiana. Results showed that Nbnrp1-RNAi lines exhibited reduced PevD1-induced immune responses, like inhibiting H
<sub>2</sub>
O
<sub>2</sub>
accumulation and MAPK phosphorylation. To silence Nbnrp1 inhibited the expression of PevD1-induced differential expression genes (DEGs) involved in pathways associated with sesquiterpenoid and triterpenoid biosynthesis, flavone and flavonol biosynthesis, plant-pathogen interaction and phenylpropanoid biosynthesis, etc. It is worth noting that sesquiterpene phytoalexin capsidiol accumulation were obviously decreased in Nbnrp1-RNAi plants after PevD1 treatment, accompanied with the down-expression of EAS and EAH, which were two key genes related to capsidiol biosynthesis. These results suggested that Nbnrp1 mediates PevD1-induced defense responses by regulating sesquiterpenoid phytoalexins biosynthesis pathway.</div>
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<AbstractText>PevD1, a fungal effector secreted by Verticillium dahliae, could induce hypersensitive responses-like necrosis and systemic acquired resistance (SAR) in cotton and tobacco plants. PevD1 could drastically induce the expression of Nbnrp1, which is an asparagine-rich protein (NRP) of Nicotiana benthamiana. Our previous research indicated that Nbnrp1 positively regulated PevD1-induced cell necrosis and disease resistance. In this study, we further investigated PevD1-induced immune responses in both wild-type (WT) and Nbnrp1-RNAi lines through RNA-seq, in order to reveal the underlying mechanism of Nbnrp1-modulated PevD1-induced disease resistance in N. benthamiana. Results showed that Nbnrp1-RNAi lines exhibited reduced PevD1-induced immune responses, like inhibiting H
<sub>2</sub>
O
<sub>2</sub>
accumulation and MAPK phosphorylation. To silence Nbnrp1 inhibited the expression of PevD1-induced differential expression genes (DEGs) involved in pathways associated with sesquiterpenoid and triterpenoid biosynthesis, flavone and flavonol biosynthesis, plant-pathogen interaction and phenylpropanoid biosynthesis, etc. It is worth noting that sesquiterpene phytoalexin capsidiol accumulation were obviously decreased in Nbnrp1-RNAi plants after PevD1 treatment, accompanied with the down-expression of EAS and EAH, which were two key genes related to capsidiol biosynthesis. These results suggested that Nbnrp1 mediates PevD1-induced defense responses by regulating sesquiterpenoid phytoalexins biosynthesis pathway.</AbstractText>
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<name sortKey="Li, Guangyue" sort="Li, Guangyue" uniqKey="Li G" first="Guangyue" last="Li">Guangyue Li</name>
<name sortKey="Li, Ze" sort="Li, Ze" uniqKey="Li Z" first="Ze" last="Li">Ze Li</name>
<name sortKey="Meng, Fanlu" sort="Meng, Fanlu" uniqKey="Meng F" first="Fanlu" last="Meng">Fanlu Meng</name>
<name sortKey="Qiu, Dewen" sort="Qiu, Dewen" uniqKey="Qiu D" first="Dewen" last="Qiu">Dewen Qiu</name>
<name sortKey="Yang, Xiufen" sort="Yang, Xiufen" uniqKey="Yang X" first="Xiufen" last="Yang">Xiufen Yang</name>
<name sortKey="Zeng, Hongmei" sort="Zeng, Hongmei" uniqKey="Zeng H" first="Hongmei" last="Zeng">Hongmei Zeng</name>
<name sortKey="Zhang, Yi" sort="Zhang, Yi" uniqKey="Zhang Y" first="Yi" last="Zhang">Yi Zhang</name>
</country>
</tree>
</affiliations>
</record>

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