Sugar metabolism drives shoot branching by repressing BRC1 through miR319-targeted TCP4 in Rosa.
Abstract
The coupling between sugar availability and shoot branching is well established, yet the underlying molecular mechanisms remain largely unknown. Here, using genome-wide profiling, we characterized the sugar signalling pathways by identifying 10 miRNAs repressed by glycolysis, the tricarboxylic acid (TCA) cycle, and/or the oxidative pentose phosphate pathway (OPPP) in rose buds. Focusing on RhmiR319, a miRNA repressed under active sugar metabolism, we demonstrate that disruption of both glycolysis/the TCA cycle and the OPPP induces the RhmiR319 accumulation, leading to the concomitant repression of its targets, RhTCP4a and RhTCP4b. We additionally reveal that the miR319/TCP4 module regulates shoot branching in Arabidopsis, as miR319 overexpression impairs shoot branching, whereas TCP4 promotes it. Altered branching patterns in Rose and Arabidopsis were associated with the expression of the branching integrator BRC1. Finally, we provide molecular evidence supporting that RhTCP4a/b directly binds to the RhBRC1 promoter and represses its transcription. Together, these results establish the miR319-TCP4-BRC1 regulatory module as a key component in the regulation of shoot branching in response to sugar status. We propose that the miR319-TCP4-BRC1 module is conserved between annual and perennial species and may integrate multiple hormonal and metabolic signals to shape shoot branching in plants.
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BibTeX
@misc{gouaille2026sugar,
title = {{Sugar metabolism drives shoot branching by repressing BRC1 through miR319-targeted TCP4 in Rosa.}},
author = {Leo Gouaille and Julie Mallet and Julie Legrix and Alexis Porcher and Laurent A Oge and Thibaut Perez and Johann Kraft and Maria-Dolores Perez-Garcia and Nathalie Leduc and Francois Barbier and Patrick Laufs and Soulaiman Sakr and Jose Le Gourrierec},
howpublished = {HAL},
year = {2026},
month = sep,
doi = {10.64898/2026.09.09.750302},
url = {https://hal.inrae.fr/hal-05749245v1},
note = {CC BY 4.0},
}
RIS
TY - UNPB
TI - Sugar metabolism drives shoot branching by repressing BRC1 through miR319-targeted TCP4 in Rosa.
AU - Leo Gouaille
AU - Julie Mallet
AU - Julie Legrix
AU - Alexis Porcher
AU - Laurent A Oge
AU - Thibaut Perez
AU - Johann Kraft
AU - Maria-Dolores Perez-Garcia
AU - Nathalie Leduc
AU - Francois Barbier
AU - Patrick Laufs
AU - Soulaiman Sakr
AU - Jose Le Gourrierec
PY - 2026
DA - 2026/09/09
PB - HAL
DO - 10.64898/2026.09.09.750302
UR - https://hal.inrae.fr/hal-05749245v1
AB - The coupling between sugar availability and shoot branching is well established, yet the underlying molecular mechanisms remain largely unknown. Here, using genome-wide profiling, we characterized the sugar signalling pathways by identifying 10 miRNAs repressed by glycolysis, the tricarboxylic acid (TCA) cycle, and/or the oxidative pentose phosphate pathway (OPPP) in rose buds. Focusing on RhmiR319, a miRNA repressed under active sugar metabolism, we demonstrate that disruption of both glycolysis/the TCA cycle and the OPPP induces the RhmiR319 accumulation, leading to the concomitant repression of its targets, RhTCP4a and RhTCP4b. We additionally reveal that the miR319/TCP4 module regulates shoot branching in Arabidopsis, as miR319 overexpression impairs shoot branching, whereas TCP4 promotes it. Altered branching patterns in Rose and Arabidopsis were associated with the expression of the branching integrator BRC1. Finally, we provide molecular evidence supporting that RhTCP4a/b directly binds to the RhBRC1 promoter and represses its transcription. Together, these results establish the miR319-TCP4-BRC1 regulatory module as a key component in the regulation of shoot branching in response to sugar status. We propose that the miR319-TCP4-BRC1 module is conserved between annual and perennial species and may integrate multiple hormonal and metabolic signals to shape shoot branching in plants.
ER -