# A GLUTAMATE CYSTEINE LIGASE Gene StGSH1 Regulated by StERF10 Enhanced Glutathione Accumulation and Adaptation to Low Phosphorus Stress in Potato

## TL;DR

A gene called StGSH1, regulated by StERF10, helps potatoes adapt to low phosphorus by boosting glutathione levels and adjusting lipid metabolism.

## Contribution

The study identifies the StERF10-StGSH1 regulatory module as a key mechanism for glutathione biosynthesis and phosphorus stress adaptation in potatoes.

## Key findings

- StGSH1 is upregulated under low phosphorus and localizes to plastids, promoting glutathione accumulation.
- StERF10 activates StGSH1, which helps maintain ROS homeostasis and facilitates lipid remodeling under low phosphorus.
- GSH biosynthesis via StGSH1 enables phosphorus use efficiency by supporting sulfolipid synthesis and phosphate release.

## Abstract

Potato (Solanum tuberosum L.) is a staple global food crop whose growth is constrained by soil phosphorus deficiency. While glutathione (GSH) modulates abiotic stress responses, its precise function and regulation in potato adaptation to low‐phosphorus (LP) remains undefined. This study demonstrated that LP triggers GSH accumulation by up‐regulating GLUTAMATE‐CYSTEINE LIGASE (StGSH1), the rate‐limiting enzyme in GSH biosynthesis. Pharmacological inhibition using buthionine sulfoximine (BSO) and exogenous GSH supplementation confirmed the essential role of GSH in LP adaptation. Confocal microscopy showed that StGSH1‐GFP fusions localize to plastids in potato protoplasts. Overexpression and silencing of StGSH1 demonstrated that it maintained reactive oxygen species (ROS) homeostasis and attenuated LP‐induced damage. StGSH1 also coordinated membrane lipid remodeling by upregulating both phospholipid catabolic genes (StNPC/PLD) and sulfolipid anabolic genes (StSQD1/2), shifting lipid flux from phosphatidylethanolamine (PE) to sulfoquinovosyldiacylglycerol (SQDG). Additionally, ETHYLENE RESPONSE FACTOR 10 (StERF10) is identified as a direct transcriptional activator of StGSH1. BSO‐mediated GSH depletion reduced the LP adaptation in StERF10‐OE plants, whereas GSH supplementation rescued StERF10‐RNAi plants, indicating StERF10 conferred LP adaptation largely through StGSH1‐mediated GSH biosynthesis. Collectively, these findings establish the StERF10‐StGSH1 module as a critical nexus connecting GSH biosynthesis to LP adaptation, providing a rational target for breeding varieties with enhanced phosphorus use efficiency.

The StERF10‐StGSH1 module coordinates glutathione (GSH) biosynthesis under low‐phosphorus stress. The low‐phosphate‐induced AP2/ERF transcription factor StERF10 directly activates the transcription of StGSH1 and enhances GSH accumulation. Consequently, GSH scavenges reactive oxygen species and provides sulfur for sulfolipid synthesis, facilitating the substitution of phospholipids and the release of phosphate Pi for plant utilization.