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Chilling of dormant buds hyperinduces FLOWERING LOCUS T and recruits GA-inducible 1,3-beta-glucanases to reopen signal conduits and release dormancy in Populus.

Identifieur interne : 002F58 ( Main/Exploration ); précédent : 002F57; suivant : 002F59

Chilling of dormant buds hyperinduces FLOWERING LOCUS T and recruits GA-inducible 1,3-beta-glucanases to reopen signal conduits and release dormancy in Populus.

Auteurs : P Ivi L H. Rinne [Norvège] ; Annikki Welling ; Jorma Vahala ; Linda Ripel ; Raili Ruonala ; Jaakko Kangasj Rvi ; Christiaan Van Der Schoot

Source :

RBID : pubmed:21282527

Descripteurs français

English descriptors

Abstract

In trees, production of intercellular signals and accessibility of signal conduits jointly govern dormancy cycling at the shoot apex. We identified 10 putative cell wall 1,3-β-glucanase genes (glucan hydrolase family 17 [GH17]) in Populus that could turn over 1,3-β-glucan (callose) at pores and plasmodesmata (PD) and investigated their regulation in relation to FT and CENL1 expression. The 10 genes encode orthologs of Arabidopsis thaliana BG_ppap, a PD-associated glycosylphosphatidylinositol (GPI) lipid-anchored protein, the Arabidopsis PD callose binding protein PDCB, and a birch (Betula pendula) putative lipid body (LB) protein. We found that these genes were differentially regulated by photoperiod, by chilling (5°C), and by feeding of gibberellins GA(3) and GA(4). GA(3) feeding upregulated all LB-associated GH17s, whereas GA(4) upregulated most GH17s with a GPI anchor and/or callose binding motif, but only GA(4) induced true bud burst. Chilling upregulated a number of GA biosynthesis and signaling genes as well as FT, but not CENL1, while the reverse was true for both GA(3) and GA(4). Collectively, the results suggest a model for dormancy release in which chilling induces FT and both GPI lipid-anchored and GA(3)-inducible GH17s to reopen signaling conduits in the embryonic shoot. When temperatures rise, the reopened conduits enable movement of FT and CENL1 to their targets, where they drive bud burst, shoot elongation, and morphogenesis.

DOI: 10.1105/tpc.110.081307
PubMed: 21282527
PubMed Central: PMC3051240


Affiliations:


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Le document en format XML

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<term>Computational Biology (MeSH)</term>
<term>Gene Expression Regulation, Plant (MeSH)</term>
<term>Gibberellins (MeSH)</term>
<term>Glucan 1,3-beta-Glucosidase (metabolism)</term>
<term>Photoperiod (MeSH)</term>
<term>Phylogeny (MeSH)</term>
<term>Plant Proteins (genetics)</term>
<term>Plant Proteins (metabolism)</term>
<term>Populus (genetics)</term>
<term>Populus (growth & development)</term>
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<term>ARN des plantes (génétique)</term>
<term>Basse température (MeSH)</term>
<term>Biologie informatique (MeSH)</term>
<term>Gibbérellines (MeSH)</term>
<term>Glucan 1,3-beta-glucosidase (métabolisme)</term>
<term>Photopériode (MeSH)</term>
<term>Phylogenèse (MeSH)</term>
<term>Populus (croissance et développement)</term>
<term>Populus (génétique)</term>
<term>Protéines végétales (génétique)</term>
<term>Protéines végétales (métabolisme)</term>
<term>Régulation de l'expression des gènes végétaux (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
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<term>Plant Proteins</term>
<term>RNA, Plant</term>
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<term>Populus</term>
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<div type="abstract" xml:lang="en">In trees, production of intercellular signals and accessibility of signal conduits jointly govern dormancy cycling at the shoot apex. We identified 10 putative cell wall 1,3-β-glucanase genes (glucan hydrolase family 17 [GH17]) in Populus that could turn over 1,3-β-glucan (callose) at pores and plasmodesmata (PD) and investigated their regulation in relation to FT and CENL1 expression. The 10 genes encode orthologs of Arabidopsis thaliana BG_ppap, a PD-associated glycosylphosphatidylinositol (GPI) lipid-anchored protein, the Arabidopsis PD callose binding protein PDCB, and a birch (Betula pendula) putative lipid body (LB) protein. We found that these genes were differentially regulated by photoperiod, by chilling (5°C), and by feeding of gibberellins GA(3) and GA(4). GA(3) feeding upregulated all LB-associated GH17s, whereas GA(4) upregulated most GH17s with a GPI anchor and/or callose binding motif, but only GA(4) induced true bud burst. Chilling upregulated a number of GA biosynthesis and signaling genes as well as FT, but not CENL1, while the reverse was true for both GA(3) and GA(4). Collectively, the results suggest a model for dormancy release in which chilling induces FT and both GPI lipid-anchored and GA(3)-inducible GH17s to reopen signaling conduits in the embryonic shoot. When temperatures rise, the reopened conduits enable movement of FT and CENL1 to their targets, where they drive bud burst, shoot elongation, and morphogenesis.</div>
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