Abstract

Selenium (Se) deficiency is widespread, yet excess inorganic Se is toxic. Enhancing plant Se through genetic biofortification is a safe strategy. Rice phosphate transporters (OsPht1) mediate selenite (SeIV) uptake, but underlying mechanisms remain unclear. In hydroponic assays, the osphf1 mutant showed significantly reduced Se accumulation, confirming OsPht1s’ involvement. The ospht1;8 and ospht1;10 mutants decreased root and shoot Se by 38.9–39.7% or 57.2–69.0%, whereas ospht1;1 reduced shoot Se by 37.2%, suggesting OsPht1;8 and OsPht1;10 mediate root Se uptake, and OsPht1;1 facilitates Se translocation. Overexpression of OsPht1;1 and OsPht1;10 enhanced shoot Se by 33.0–55.4%, whereas OsPht1;8 overexpression increased root Se by 32.3–36.2% and reduced Cd by 26.6–35.1% in shoots and 27.6–41.5% in grains through elevated cysteine and enhanced OsHMA3 and OsPCS2 expression. These findings demonstrate distinct roles of OsPht1 members in Se accumulation, providing candidate genes for breeding Se-enriched rice, with OsPht1;8 additionally lowering Cd risk.