Year: 2026
Type: preprint
Abstract: Disorder can localize valence- and conduction-band states to different degrees, yet whether such localization contrast has observable consequences remains poorly understood. Here, we show that localization contrast strongly impacts competing carrier-recombination channels. We illustrate this behavior in random In$_x$Ga$_{1-x}$N alloys. Increasing the In content from $x=13.5\%$ to $x=22\%$ progressively localizes the valence-band maximum state while leaving the conduction-band minimum state comparatively delocalized. This contrasting localization decreases the interband optical momentum matrix element underlying radiative recombination. For Auger-Meitner recombination, however, localization alone does not determine the coupling; atomic-scale disorder also breaks primitive-cell translational symmetry and modifies the momentum-space and phase structure of the states. This generates additional low-$Q$ components and enhances the Auger coupling by more than five orders of magnitude relative to pristine GaN. Thus, we provide a microscopic explanation for the competing trends in radiative and Auger recombination. More broadly, our results establish localization contrast as a mechanism through which disorder can control optical and carrier-carrier interactions in semiconductors.
Source: arXiv (Cornell University)
Institution: University of California, Santa Barbara
Language: English
Subfield: Condensed Matter Physics
Field: Physics and Astronomy
Domain: Physical Sciences
Open Access status: green
Awards: G1453181110, Track 4: Advanced CI Coordination Ecosystem: Monitoring and Measurement Services, G243532934, G2465863988, G3562386289, Track 1: ACCESS Resource Allocations Marketplace and Platform Services (RAMPS), G4010157413, ACO: An Open CI Ecosystem to Advance Scientific Discovery (OpenCI), Track 3: COre National Ecosystem for CyberinfrasTructure (CONECT), G5367127336, G5464919783, Track 2: Customized Multi-tier Assistance, Training, and Computational Help (MATCH) for End User ACCESS to CI
OpenAlex ID: W7223334794