Abstract

Globally, 94–220 million people in regions with arsenic (As)-contaminated soil or groundwater face significant health risks. Rice, the primary staple food in these areas, is the main source of As exposure for a large portion of this population. Developing low-As rice cultivars provides a sustainable strategy to reduce dietary As exposure. However, As uptake in rice shares pathways with nutrient uptake, such as phosphate (P) transporters. The lack of As-specific transporters makes it challenging to reduce As accumulation in plants by regulating As uptake genes, as such approaches risk disrupting P uptake and plant growth. Here, we functionally characterized two phosphate transporter genes, OsPht1;9 / OsPht1;10 , which play a key role in arsenate (AsV) uptake and translocation in rice but minimally contribute to P utilization. Under hydroponic conditions, the double mutants of OsPht1;9 / 1;10 exhibited a 46.2–65.7% reduction in shoot As accumulation, with the As concentrations in xylem sap being 16.5–34.8% lower than the wild type controls. In multi-year field trials at two locations, simultaneous knockout of OsPht1;9 / 1;10 significantly decreased grain As concentration by 19.2–47.3%, without compromising yield. This study identifies novel gene-editing targets for low-As rice development and provides a breakthrough in mitigating As contamination exposure while enhancing food safety.