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Abstract The performance of electronic and optoelectronic devices is dominated by charge carrier injection through the metal–semiconductor contacts. Therefore, creating low-resistance electrical contacts is one of the most critical challenges in the development of devices based on new materials, particularly in the case of two-dimensional semiconductors. Herein, we report a strategy to reduce the contact resistance of MoS 2 via local pressurization. We fabricated electrical contacts using an atomic force microscopy tip and applied variable pressure ranging from 0 to 25 GPa. By measuring the transverse electronic transport properties, we show that MoS 2 undergoes a reversible semiconducting-metallic transition under pressure. Planar devices in field effect configuration with electrical contacts performed at pressures above ∼15 GPa show up to 30-fold reduced contact resistance and up to 25-fold improved field-effect mobility when compared to those measured at low pressure. Theoretical simulations show that this enhanced performance is due to improved charge injection to the MoS 2 semiconductor channel through the metallic MoS 2 phase obtained by pressurization. Our results suggest a novel strategy for realizing improved contacts to MoS 2 devices by local pressurization and for exploring emergent phenomena under mechano-electric modulation. 

Summary Arsenic poses a global threat to living organisms, compromising crop security and yield. Limited understanding of the transcriptional network integrating arsenic‐tolerance mechanisms with plant developmental responses hinders the development of strategies against this toxic metalloid.Here, we conducted a high‐throughput yeast one‐hybrid assay using as baits the promoter region from the arsenic‐inducible genesARQ1andASK18fromArabidopsis thaliana, coupled with a transcriptomic analysis, to uncover novel transcriptional regulators of the arsenic response.We identified the GLABRA2 (GL2) transcription factor as a novel regulator of arsenic tolerance, revealing a wider regulatory role beyond its established function as a repressor of root hair formation. Furthermore, we found that ANTHOCYANINLESS2 (ANL2), a GL2 subfamily member, acts redundantly with this transcription factor in the regulation of arsenic signaling. Both transcription factors act as repressors of arsenic response.gl2andanl2mutants exhibit enhanced tolerance and reduced arsenic accumulation. Transcriptional analysis in thegl2mutant unveils potential regulators of arsenic tolerance.These findings highlight GL2 and ANL2 as novel integrators of the arsenic response with developmental outcomes, offering insights for developing safer crops with reduced arsenic content and increased tolerance to this hazardous metalloid.