Strigolactone signalling inhibits trehalose 6‐phosphate signalling independently of BRC1 to suppress shoot branching

Author:

Fichtner Franziska12345ORCID,Humphreys Jazmine L.6ORCID,Barbier Francois F.127ORCID,Feil Regina5ORCID,Westhoff Philipp4ORCID,Moseler Anna8ORCID,Lunn John E.5ORCID,Smith Steven M.6ORCID,Beveridge Christine A.12ORCID

Affiliation:

1. School of Agriculture and Food Sustainability The University of Queensland St Lucia QLD 4072 Australia

2. ARC Centre for Plant Success in Nature and Agriculture The University of Queensland St Lucia QLD 4072 Australia

3. Faculty of Mathematics and Natural Sciences Institute of Plant Biochemistry, Heinrich Heine University Düsseldorf Düsseldorf 40225 Germany

4. Cluster of Excellence in Plant Science (CEPLAS) Heinrich Heine University Düsseldorf 40225 Germany

5. Max Planck Institute of Molecular Plant Physiology Potsdam‐Golm 14476 Germany

6. ARC Centre for Plant Success in Nature and Agriculture, School of Natural Sciences University of Tasmania Hobart TAS 7001 Australia

7. Institute for Plant Sciences of Montpellier University of Montpellier, CNRS, INRAe, Institut Agro Montpellier 34060 France

8. INRES‐Chemical Signalling University of Bonn Bonn 53113 Germany

Abstract

Summary The phytohormone strigolactone (SL) inhibits shoot branching, whereas the signalling metabolite trehalose 6‐phosphate (Tre6P) promotes branching. How Tre6P and SL signalling may interact and which molecular mechanisms might be involved remains largely unknown. Transcript profiling of Arabidopsis SL mutants revealed a cluster of differentially expressed genes highly enriched in the Tre6P pathway compared with wild‐type (WT) plants or brc1 mutants. Tre6P‐related genes were also differentially expressed in axillary buds of garden pea (Pisum sativum) SL mutants. Tre6P levels were elevated in the SL signalling mutant more axillary (max) growth 2 compared with other SL mutants or WT plants indicating a role of MAX2‐dependent SL signalling in regulating Tre6P levels. A transgenic approach to increase Tre6P levels demonstrated that all SL mutant lines and brc1 flowered earlier, showing all of these mutants were responsive to Tre6P. Elevated Tre6P led to increased branching in WT plants but not in max2 and max4 mutants, indicating some dependency between the SL pathway and Tre6P regulation of shoot branching. By contrast, elevated Tre6P led to an enhanced branching phenotype in brc1 mutants indicating independence between BRC1 and Tre6P. A model is proposed whereby SL signalling represses branching via Tre6P and independently of the BRC1 pathway.

Funder

Max-Planck-Gesellschaft

Australian Research Council

Deutsche Forschungsgemeinschaft

Publisher

Wiley

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