# SWEET1‐mediated glucose transport is crucial for energy availability in Arabidopsis

## TL;DR

This study shows that the SWEET1 transporter helps glucose counteract the effects of the stress hormone ABA during seed germination in Arabidopsis.

## Contribution

The study identifies SWEET1 as the key glucose transporter that mediates glucose signaling to suppress ABA inhibition during germination.

## Key findings

- SWEET1 is essential for glucose transport that counteracts ABA-induced germination inhibition.
- sweet1 mutants show delayed germination and reduced glucose transport under ABA treatment.
- Glc signaling through the SnRK1 kinase pathway, including KIN10, partially mediates this suppression.

## Abstract

The stress‐responsive hormone abscisic acid (ABA) is known for its inhibitory effects on various physiological processes, including seed germination, often resulting in energy deprivation. Interestingly, ABA‐induced germination inhibition can be alleviated by exogenous glucose (Glc), mimicking a functional interplay between ABA and sugar signaling in vivo. However, it remains poorly understood which sugar transporter mediates Glc allocation under ABA treatment and how Glc counteracts the effects of ABA.To address this, we combined transcriptomic analyses, transport assays, physiological studies, and genetic approaches to identify and characterize processes involved in Glc allocation that counteract the inhibitory effects of ABA during seed germination in Arabidopsis thaliana.We identified the plasma membrane‐localized Glc uniporter SWEET1 as a key player in the Glc‐mediated suppression of ABA inhibition. The sweet1 mutants showed delayed germination in the presence of ABA, reduced Glc transport, and slower root growth under energy starvation conditions. The suppression of ABA inhibited germination by Glc transported by SWEET1 appears to depend, at least partially, on Glc signaling through SnRK1 kinase pathway, including KIN10.Our findings demonstrate that SWEET1 is crucial for Glc suppression of ABA‐induced inhibition during seed germination and provide insight into sugar signaling pathways linked to environment‐ or ABA‐triggered energy deficiency.

The stress‐responsive hormone abscisic acid (ABA) is known for its inhibitory effects on various physiological processes, including seed germination, often resulting in energy deprivation. Interestingly, ABA‐induced germination inhibition can be alleviated by exogenous glucose (Glc), mimicking a functional interplay between ABA and sugar signaling in vivo. However, it remains poorly understood which sugar transporter mediates Glc allocation under ABA treatment and how Glc counteracts the effects of ABA.

To address this, we combined transcriptomic analyses, transport assays, physiological studies, and genetic approaches to identify and characterize processes involved in Glc allocation that counteract the inhibitory effects of ABA during seed germination in Arabidopsis thaliana.

We identified the plasma membrane‐localized Glc uniporter SWEET1 as a key player in the Glc‐mediated suppression of ABA inhibition. The sweet1 mutants showed delayed germination in the presence of ABA, reduced Glc transport, and slower root growth under energy starvation conditions. The suppression of ABA inhibited germination by Glc transported by SWEET1 appears to depend, at least partially, on Glc signaling through SnRK1 kinase pathway, including KIN10.

Our findings demonstrate that SWEET1 is crucial for Glc suppression of ABA‐induced inhibition during seed germination and provide insight into sugar signaling pathways linked to environment‐ or ABA‐triggered energy deficiency.