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Overexpression of PeMIPS1 confers tolerance to salt and copper stresses by scavenging reactive oxygen species in transgenic poplar.

Identifieur interne : 000D57 ( Main/Exploration ); précédent : 000D56; suivant : 000D58

Overexpression of PeMIPS1 confers tolerance to salt and copper stresses by scavenging reactive oxygen species in transgenic poplar.

Auteurs : Jing Zhang [République populaire de Chine] ; Nan Yang [République populaire de Chine] ; Yuanyuan Li [République populaire de Chine] ; Shidong Zhu [République populaire de Chine] ; Shengnan Zhang [République populaire de Chine] ; Yadong Sun [République populaire de Chine] ; Hong-Xia Zhang [République populaire de Chine] ; Lei Wang [République populaire de Chine] ; Hongyan Su [République populaire de Chine]

Source :

RBID : pubmed:29579299

Descripteurs français

English descriptors

Abstract

Myo-inositol is a vital compound in plants. As the key rate-limiting enzyme in myo-inositol biosynthesis, l-myo-inositol-1-phosphate synthase (MIPS) is regarded as a determinant of the myo-inositol content in plants. The up-regulation of MIPS genes can increase the myo-inositol content, thereby enhancing the plant's resistance to a variety of stresses. However, there are few reports on the roles of myo-inositol and the identification of MIPS in woody trees. In this study, a MIPS gene, named as PeMIPS1, was characterized from Populus euphratica Oliv. The heterologous expression of PeMIPS1 compensated for inositol production in the yeast inositol auxotrophic mutant ino1 and the phenotypic lesions of the atmips1-2 mutant, an Arabidopsis MIPS1 knock-out mutant. A subcellular location analysis showed that the PeMIPS1-GFP fusion was localized in the nucleus and cytoplasm, but not in the chloroplasts, indicating that PeMIPS1 represented the cytosolic form of MIPS in P. euphratica. Interestingly, PeMIPS1 was not only inducible by drought and high salinity, but also by CuSO4 treatment. The transgenic poplar lines overexpressing PeMIPS1 had greater plant heights, shoot biomasses and survival rates than the wild type during the salt- or copper-stress treatment, and this was accompanied by an increase in the myo-inositol content. The overexpression of PeMIPS1 resulted in the increased activities of antioxidant enzymes and the accumulation of ascorbate, a key nonenzymatic antioxidant in plant, which partly accounted for the enhanced reactive oxygen species-scavenging capacity and the lowered hydrogen peroxide and malondialdehyde levels in the transgenic poplar. To the best of our knowledge, this study is the first to report the roles of MIPS genes in the tolerance to copper stress.

DOI: 10.1093/treephys/tpy028
PubMed: 29579299


Affiliations:


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Le document en format XML

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<term>Copper (metabolism)</term>
<term>Gene Expression Regulation, Plant (MeSH)</term>
<term>Myo-Inositol-1-Phosphate Synthase (genetics)</term>
<term>Myo-Inositol-1-Phosphate Synthase (metabolism)</term>
<term>Plants, Genetically Modified (genetics)</term>
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<term>Populus (physiology)</term>
<term>Reactive Oxygen Species (metabolism)</term>
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<term>Soil Pollutants (metabolism)</term>
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<term>Cuivre (métabolisme)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Myo-inositol 1-phosphate synthase (génétique)</term>
<term>Myo-inositol 1-phosphate synthase (métabolisme)</term>
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<term>Populus (physiologie)</term>
<term>Régulation de l'expression des gènes végétaux (MeSH)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Stress physiologique (MeSH)</term>
<term>Tolérance au sel (MeSH)</term>
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<term>Myo-Inositol-1-Phosphate Synthase</term>
<term>Reactive Oxygen Species</term>
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<div type="abstract" xml:lang="en">Myo-inositol is a vital compound in plants. As the key rate-limiting enzyme in myo-inositol biosynthesis, l-myo-inositol-1-phosphate synthase (MIPS) is regarded as a determinant of the myo-inositol content in plants. The up-regulation of MIPS genes can increase the myo-inositol content, thereby enhancing the plant's resistance to a variety of stresses. However, there are few reports on the roles of myo-inositol and the identification of MIPS in woody trees. In this study, a MIPS gene, named as PeMIPS1, was characterized from Populus euphratica Oliv. The heterologous expression of PeMIPS1 compensated for inositol production in the yeast inositol auxotrophic mutant ino1 and the phenotypic lesions of the atmips1-2 mutant, an Arabidopsis MIPS1 knock-out mutant. A subcellular location analysis showed that the PeMIPS1-GFP fusion was localized in the nucleus and cytoplasm, but not in the chloroplasts, indicating that PeMIPS1 represented the cytosolic form of MIPS in P. euphratica. Interestingly, PeMIPS1 was not only inducible by drought and high salinity, but also by CuSO4 treatment. The transgenic poplar lines overexpressing PeMIPS1 had greater plant heights, shoot biomasses and survival rates than the wild type during the salt- or copper-stress treatment, and this was accompanied by an increase in the myo-inositol content. The overexpression of PeMIPS1 resulted in the increased activities of antioxidant enzymes and the accumulation of ascorbate, a key nonenzymatic antioxidant in plant, which partly accounted for the enhanced reactive oxygen species-scavenging capacity and the lowered hydrogen peroxide and malondialdehyde levels in the transgenic poplar. To the best of our knowledge, this study is the first to report the roles of MIPS genes in the tolerance to copper stress.</div>
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</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList>
<MeshHeading>
<DescriptorName UI="D017360" MajorTopicYN="N">Arabidopsis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D003300" MajorTopicYN="N">Copper</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018506" MajorTopicYN="Y">Gene Expression Regulation, Plant</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D007296" MajorTopicYN="N">Myo-Inositol-1-Phosphate Synthase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D030821" MajorTopicYN="N">Plants, Genetically Modified</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D032107" MajorTopicYN="N">Populus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D055049" MajorTopicYN="Y">Salt Tolerance</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D012989" MajorTopicYN="N">Soil Pollutants</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
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<History>
<PubMedPubDate PubStatus="received">
<Year>2017</Year>
<Month>10</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2018</Year>
<Month>02</Month>
<Day>23</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed">
<Year>2018</Year>
<Month>3</Month>
<Day>27</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2019</Year>
<Month>2</Month>
<Day>8</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2018</Year>
<Month>3</Month>
<Day>27</Day>
<Hour>6</Hour>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
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<ArticleId IdType="pubmed">29579299</ArticleId>
<ArticleId IdType="pii">4951457</ArticleId>
<ArticleId IdType="doi">10.1093/treephys/tpy028</ArticleId>
</ArticleIdList>
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</pubmed>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
</list>
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<country name="République populaire de Chine">
<noRegion>
<name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name>
</noRegion>
<name sortKey="Li, Yuanyuan" sort="Li, Yuanyuan" uniqKey="Li Y" first="Yuanyuan" last="Li">Yuanyuan Li</name>
<name sortKey="Su, Hongyan" sort="Su, Hongyan" uniqKey="Su H" first="Hongyan" last="Su">Hongyan Su</name>
<name sortKey="Sun, Yadong" sort="Sun, Yadong" uniqKey="Sun Y" first="Yadong" last="Sun">Yadong Sun</name>
<name sortKey="Wang, Lei" sort="Wang, Lei" uniqKey="Wang L" first="Lei" last="Wang">Lei Wang</name>
<name sortKey="Yang, Nan" sort="Yang, Nan" uniqKey="Yang N" first="Nan" last="Yang">Nan Yang</name>
<name sortKey="Zhang, Hong Xia" sort="Zhang, Hong Xia" uniqKey="Zhang H" first="Hong-Xia" last="Zhang">Hong-Xia Zhang</name>
<name sortKey="Zhang, Shengnan" sort="Zhang, Shengnan" uniqKey="Zhang S" first="Shengnan" last="Zhang">Shengnan Zhang</name>
<name sortKey="Zhu, Shidong" sort="Zhu, Shidong" uniqKey="Zhu S" first="Shidong" last="Zhu">Shidong Zhu</name>
</country>
</tree>
</affiliations>
</record>

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