Point defect engineering is widely used to tailor the electronic and transport properties of complex oxides, yet its influence on dislocation plasticity remains poorly understood. Here, we establish how donor (Nb) doping modifies dislocation nucleation, multiplication, and mobility in single-crystal SrTiO₃ by bridging nano-, meso-, and macroscale deformation. Using a combinatorial approach involving nanoindentation, cyclic Brinell indentation, and bulk uniaxial compression, we show that 0.5 wt% Nb doping consistently suppresses room-temperature plasticity. Nanoindentation reveals increased pop-in stresses, increased lattice friction stress, and reduced creep rates, indicating inhibited dislocation nucleation and motion with Nb doping. Mesoscale Brinell indentation exhibits discrete, widely spaced slip traces reflecting more difficult dislocation multiplication. Bulk uniaxial compression confirms ∼50% higher yield stress in Nb-doped (0.5 wt%) SrTiO₃ samples, which underscores the strength-plasticity tradeoff. Comparison with Fe-doped SrTiO₃ (equivalent doping concentration) isolates the role of defect chemistry: oxygen vacancies promote incipient plasticity, whereas Sr vacancies dominate in Nb-doped SrTiO₃, strongly hindering dislocation motion. This length-scale bridging approach consistently reveals suppressed dislocation nucleation, multiplication, and motion in the 0.5 wt% Nb-doped samples. These insights underline the importance of dislocation-defect chemistry on the mechanical behavior of functional oxides.