Key message <p>The mitochondrial gene <i>ORF188</i> enhances salt stress tolerance in rapeseed by boosting ATP synthesis, thereby fueling antioxidant defense systems and maintaining cellular homeostasis.</p> Abstract <p>Soil salinity severely impairs crop productivity by inducing osmotic stress, ionic toxicity, and oxidative damage. An energy deficit, arising from impaired mitochondrial ATP production under stress, represents a critical bottleneck that compromises the plant’s antioxidant capacity. Here, we report that the mitochondrial gene <i>ORF188</i>, a homolog of the ATP synthase F₀ subunit, significantly enhances salt stress tolerance in rapeseed. <i>ORF188</i>-overexpressing lines exhibited superior growth and reduced oxidative damage under salt stress, which was underpinned by constitutively elevated ATP synthase activity and cellular ATP levels. This energy surplus enhanced the antioxidant system, maintained favorable Na⁺/K⁺ ratio and orchestrated a homeostasis-oriented stress transcriptome. Crucially, treatment with the ATP synthase inhibitor Oligomycin A abolished both the salt-tolerant phenotype and the associated transcriptional reprogramming, thereby confirming the essential role of enhanced ATP synthesis. Our findings demonstrate that <i>ORF188</i> as a key genetic determinant of salt stress tolerance via ATP-dependent antioxidant activation, and representing a promising target for breeding salt-resilient crops.</p>