Truncated BAM receptors interfere the apical meristematic activity in a dominant negative manner when ectopically expressed in Arabidopsis.
Identifieur interne : 000C16 ( Main/Exploration ); précédent : 000C15; suivant : 000C17Truncated BAM receptors interfere the apical meristematic activity in a dominant negative manner when ectopically expressed in Arabidopsis.
Auteurs : Caili Wang [République populaire de Chine] ; Heyu Yang [République populaire de Chine] ; Lincai Chen [République populaire de Chine] ; Shaohui Yang [République populaire de Chine] ; Deping Hua [République populaire de Chine] ; Jiehua Wang [République populaire de Chine]Source :
- Plant science : an international journal of experimental plant biology [ 1873-2259 ] ; 2018.
Descripteurs français
- KwdFr :
- Arabidopsis (croissance et développement), Arabidopsis (génétique), Arabidopsis (métabolisme), Expression génique ectopique (MeSH), Méristème (croissance et développement), Méristème (génétique), Méristème (métabolisme), Populus (croissance et développement), Populus (génétique), Populus (métabolisme), Pousses de plante (croissance et développement), Pousses de plante (génétique), Pousses de plante (métabolisme), Protein-Serine-Threonine Kinases (génétique), Protein-Serine-Threonine Kinases (métabolisme), Protéines d'Arabidopsis (génétique), Protéines d'Arabidopsis (métabolisme), Régulation de l'expression des gènes végétaux (MeSH), Transduction du signal (MeSH), Végétaux génétiquement modifiés (génétique), Végétaux génétiquement modifiés (métabolisme).
- MESH :
- croissance et développement : Arabidopsis, Méristème, Populus, Pousses de plante.
- génétique : Arabidopsis, Méristème, Populus, Pousses de plante, Protein-Serine-Threonine Kinases, Protéines d'Arabidopsis, Végétaux génétiquement modifiés.
- métabolisme : Arabidopsis, Méristème, Populus, Pousses de plante, Protein-Serine-Threonine Kinases, Protéines d'Arabidopsis, Végétaux génétiquement modifiés.
- Expression génique ectopique, Régulation de l'expression des gènes végétaux, Transduction du signal.
English descriptors
- KwdEn :
- Arabidopsis (genetics), Arabidopsis (growth & development), Arabidopsis (metabolism), Arabidopsis Proteins (genetics), Arabidopsis Proteins (metabolism), Ectopic Gene Expression (MeSH), Gene Expression Regulation, Plant (MeSH), Meristem (genetics), Meristem (growth & development), Meristem (metabolism), Plant Shoots (genetics), Plant Shoots (growth & development), Plant Shoots (metabolism), Plants, Genetically Modified (genetics), Plants, Genetically Modified (metabolism), Populus (genetics), Populus (growth & development), Populus (metabolism), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (metabolism), Signal Transduction (MeSH).
- MESH :
- chemical , genetics : Arabidopsis Proteins, Protein-Serine-Threonine Kinases.
- genetics : Arabidopsis, Meristem, Plant Shoots, Plants, Genetically Modified, Populus.
- growth & development : Arabidopsis, Meristem, Plant Shoots, Populus.
- metabolism : Arabidopsis, Arabidopsis Proteins, Meristem, Plant Shoots, Plants, Genetically Modified, Populus, Protein-Serine-Threonine Kinases.
- Ectopic Gene Expression, Gene Expression Regulation, Plant, Signal Transduction.
Abstract
Small, secreted signaling peptides that are perceived by receptor-like kinases (RLKs) constitute an important regulatory mechanism in plant organ formation and stem cell maintenance. However, functional redundancy at the level of both ligand and receptor families often makes it difficult to clearly discern the role of individual members by a genetic approach. Here, we show that driven by a constitutive CaMV 35S promoter, a truncated BAM protein (BAMΔ) that lacks either the signal peptide (SP) or the cytoplasmic kinase (Ki) domain could cause defective shoot apical meristem (SAM) maintenance, which phenotypically resembled the triple bam mutant. Such a dominant-negative effect could also be achieved when the same transgene was driven by the native AtBAM1 promoter, but not by the CLV1 promoter. When introduced into a clv1-4 background, BAMΔ proteins abolished the typical clv phenotype by suppressing the transcriptional level of clv1-4. In addition to a clear reduction in root length and a decreased number of meristematic cells, the 35S:BAMΔ transgenic seedlings exhibited considerable resistance to CLE40p- but not to CLV3p-mediated root growth inhibition, implying that BAMs play key roles in the regulation of proximal meristem activity in root through CLE40 peptide. Findings present here not only provide evidence that truncated BAM proteins are strongly dominant negative in regulating apical meristem development but also propose that expression of a truncated version of plant LRR receptor kinase could potentially be used as a powerful tool to reveal its in vivo function in signal transduction.
DOI: 10.1016/j.plantsci.2018.01.003
PubMed: 29606214
Affiliations:
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However, functional redundancy at the level of both ligand and receptor families often makes it difficult to clearly discern the role of individual members by a genetic approach. Here, we show that driven by a constitutive CaMV 35S promoter, a truncated BAM protein (BAMΔ) that lacks either the signal peptide (SP) or the cytoplasmic kinase (Ki) domain could cause defective shoot apical meristem (SAM) maintenance, which phenotypically resembled the triple bam mutant. Such a dominant-negative effect could also be achieved when the same transgene was driven by the native AtBAM1 promoter, but not by the CLV1 promoter. When introduced into a clv1-4 background, BAMΔ proteins abolished the typical clv phenotype by suppressing the transcriptional level of clv1-4. In addition to a clear reduction in root length and a decreased number of meristematic cells, the 35S:BAMΔ transgenic seedlings exhibited considerable resistance to CLE40p- but not to CLV3p-mediated root growth inhibition, implying that BAMs play key roles in the regulation of proximal meristem activity in root through CLE40 peptide. Findings present here not only provide evidence that truncated BAM proteins are strongly dominant negative in regulating apical meristem development but also propose that expression of a truncated version of plant LRR receptor kinase could potentially be used as a powerful tool to reveal its in vivo function in signal transduction.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29606214</PMID><DateCompleted><Year>2018</Year><Month>08</Month><Day>27</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-2259</ISSN><JournalIssue CitedMedium="Internet"><Volume>269</Volume><PubDate><Year>2018</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Plant science : an international journal of experimental plant biology</Title><ISOAbbreviation>Plant Sci</ISOAbbreviation></Journal><ArticleTitle>Truncated BAM receptors interfere the apical meristematic activity in a dominant negative manner when ectopically expressed in Arabidopsis.</ArticleTitle><Pagination><MedlinePgn>20-31</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0168-9452(17)31044-0</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.plantsci.2018.01.003</ELocationID><Abstract><AbstractText>Small, secreted signaling peptides that are perceived by receptor-like kinases (RLKs) constitute an important regulatory mechanism in plant organ formation and stem cell maintenance. However, functional redundancy at the level of both ligand and receptor families often makes it difficult to clearly discern the role of individual members by a genetic approach. Here, we show that driven by a constitutive CaMV 35S promoter, a truncated BAM protein (BAMΔ) that lacks either the signal peptide (SP) or the cytoplasmic kinase (Ki) domain could cause defective shoot apical meristem (SAM) maintenance, which phenotypically resembled the triple bam mutant. Such a dominant-negative effect could also be achieved when the same transgene was driven by the native AtBAM1 promoter, but not by the CLV1 promoter. When introduced into a clv1-4 background, BAMΔ proteins abolished the typical clv phenotype by suppressing the transcriptional level of clv1-4. In addition to a clear reduction in root length and a decreased number of meristematic cells, the 35S:BAMΔ transgenic seedlings exhibited considerable resistance to CLE40p- but not to CLV3p-mediated root growth inhibition, implying that BAMs play key roles in the regulation of proximal meristem activity in root through CLE40 peptide. Findings present here not only provide evidence that truncated BAM proteins are strongly dominant negative in regulating apical meristem development but also propose that expression of a truncated version of plant LRR receptor kinase could potentially be used as a powerful tool to reveal its in vivo function in signal transduction.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Caili</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>School of Environmental Science and Engineerin, Tianjin University, Tianjin 300072, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Heyu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>School of Environmental Science and Engineerin, Tianjin University, Tianjin 300072, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Lincai</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>School of Environmental Science and Engineerin, Tianjin University, Tianjin 300072, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Shaohui</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>School of Environmental Science and Engineerin, Tianjin University, Tianjin 300072, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hua</LastName><ForeName>Deping</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>School of Life Sciences, Tianjin University, Tianjin 300072, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jiehua</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>School of Environmental Science and Engineerin, Tianjin University, Tianjin 300072, China. Electronic address: jiehuawang@tju.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>02</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Plant Sci</MedlineTA><NlmUniqueID>9882015</NlmUniqueID><ISSNLinking>0168-9452</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029681">Arabidopsis Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C519658">BAM1 protein, Arabidopsis</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C118166">CLV1 protein, Arabidopsis</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D017346">Protein-Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017360" MajorTopicYN="N">Arabidopsis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029681" MajorTopicYN="N">Arabidopsis Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000066630" MajorTopicYN="Y">Ectopic Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018506" MajorTopicYN="Y">Gene Expression Regulation, Plant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018519" MajorTopicYN="N">Meristem</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018520" MajorTopicYN="N">Plant Shoots</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D030821" MajorTopicYN="N">Plants, Genetically Modified</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D032107" MajorTopicYN="N">Populus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Arabidopsis thaliana</Keyword><Keyword MajorTopicYN="N">CLE signaling</Keyword><Keyword MajorTopicYN="N">Negative dominant</Keyword><Keyword MajorTopicYN="N">Shoot apical meristem</Keyword><Keyword MajorTopicYN="N">Truncated LRR receptor kinase</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>11</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>01</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>01</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>4</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>4</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>8</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29606214</ArticleId><ArticleId IdType="pii">S0168-9452(17)31044-0</ArticleId><ArticleId IdType="doi">10.1016/j.plantsci.2018.01.003</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Tianjin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wang, Caili" sort="Wang, Caili" uniqKey="Wang C" first="Caili" last="Wang">Caili Wang</name></noRegion><name sortKey="Chen, Lincai" sort="Chen, Lincai" uniqKey="Chen L" first="Lincai" last="Chen">Lincai Chen</name><name sortKey="Hua, Deping" sort="Hua, Deping" uniqKey="Hua D" first="Deping" last="Hua">Deping Hua</name><name sortKey="Wang, Jiehua" sort="Wang, Jiehua" uniqKey="Wang J" first="Jiehua" last="Wang">Jiehua Wang</name><name sortKey="Yang, Heyu" sort="Yang, Heyu" uniqKey="Yang H" first="Heyu" last="Yang">Heyu Yang</name><name sortKey="Yang, Shaohui" sort="Yang, Shaohui" uniqKey="Yang S" first="Shaohui" last="Yang">Shaohui Yang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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