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Plant roots are essential organs for absorbing nutrients from the soil or medium. Sucrose functions as a vital carbon source in root development, and sucrose starvation interferes with the redox state of plant cells. However, the mechanism of root growth at sucrose starvation remains unclear. Here, we report that SHMT1 (serine hydroxymethyltransferase 1) plays a crucial role in primary-root growth. <i>SHMT1</i> mutation caused decreased sugar levels, excessive H₂O₂ accumulation, and severe root-growth arrest at sucrose-free conditions, whereas plants with <i>SHMT1</i> overexpression had increased sugar and decreased H₂O₂ levels, and longer primary roots. Sucrose supply fully restored root growth of <i>shm1-2</i>, but CO₂ alone could not, and SHMT1 is much more stable in roots than shoots at sucrose conditions, suggesting that SHMT1 accumulation in roots is critical for sucrose accumulation and root growth. Further ROS scavenging by GSH application or ROS synthesis inhibition by apocynin application or <i>RBOHD</i> mutation reduced H₂O₂ levels and partially restored the root-growth arrest phenotype of <i>shm1-2</i> at low-sucrose conditions, suggesting that SHMT1 modulates root growth via sucrose-mediated ROS accumulation. Our findings demonstrated the role of SHMT1 in primary-root growth by regulating sucrose accumulation and ROS homeostasis in roots.