Rice （Oryza sativa L.）， a critical cereal crop sustaining global food security， faces severe yield limitations due to soil alkalinity. Enhancing the salt-alkali tolerance of rice varieties represents a pivotal strategy for boosting overall production and ensuring food security through expanding cultivable land in saline-alkaline environments. In this study， a mutant M23 with significantly reduced alkaline tolerance was identified from the γ-ray induced mutation library of the Japonica rice variety Sasanishiki （WT）. Following a map-based cloning strategy， the target gene was allocated in an 87.7 kb region between markers P2 and P3 on chromosome 11， containing nine open reading frames （ORFs）. Sequence comparison revealed a four base pair deletion in the third exon of ORF9 in the mutant， leading to premature termination. Therefore， ORF9 is hypothesized to be the strong candidate gene， designated Alkaline Tolerance 11 （AT11）， which encodes a putative peptide transporter （PTR）. CRISPR/Cas9 knockout lines of AT11 showed decreased alkaline tolerance， whereas its overexpression significantly enhanced alkaline tolerance. AT11 is expressed in all tissues with the highest expression in the panicle in rice. Yeast two-hybrid （Y2H） assay and Immunoprecipitation assay revealed that AT11 can interact with GS3， the heterotrimeric G-protein γ subunit in rice. Bimolecular fluorescence complementation （BiFC） experiments pointed out their interaction on the plasma membrane. Through transcriptome sequencing analysis， the differentially expressed genes between WT and AT11 knockout lines were significantly enriched in pigment binding and photosynthesis. Yield testing under field conditions at pH=9.0 showed that AT11 overexpression significantly increased yield production， demonstrating that AT11 can enhance the productivity of rice on saline-alkaline soils， with a potential for rice breeding with salt alkaline resistance.