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Spin qubits in gate-defined silicon quantum dots are receiving increased attention thanks to their potential for large-scale quantum computing. Readout of such spin qubits is done most accurately and scalably via Pauli spin blockade (PSB), however, various mechanisms may lift PSB and complicate readout. In this work, we present an experimental study of PSB in a multi-electron low-symmetry double quantum dot (DQD) in silicon nanowires. We report on the observation of non-symmetric PSB, manifesting as blockaded tunneling when the spin is projected to one QD of the pair but as allowed tunneling when the projection is done into the other. By analyzing the interaction of the DQD with a readout resonator, we find that PSB lifting is caused by a large coupling between the different electron spin manifolds of 7.90 μeV and that tunneling is incoherent. Further, magnetospectroscopy of the DQD in 16 charge configurations, enables reconstructing the energy spectrum of the DQD and reveals the lifting mechanism is energy-level selective. Our results indicate enhanced spin-orbit coupling which may enable all-electrical qubit control of electron spins in silicon nanowires. [ABSTRACT FROM AUTHOR]

Introduction: The Hippo pathway and its transcriptional effectors yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are targets for cancer therapy. It is important to determine if the activation of one factor compensates for the inhibition of the other. Moreover, it is unknown if YAP/TAZ-directed perturbation affects cell–cell communication of non-malignant liver cells. Materials and Methods: To investigate liver-specific phenotypes caused by YAP and TAZ inactivation, we generated mice with hepatocyte (HC) and biliary epithelial cell (BEC)-specific deletions for both factors (YAPKO, TAZKO and double knock-out (DKO)). Immunohistochemistry, single-cell sequencing, and proteomics were used to analyze liver tissues and serum. Results: The loss of BECs, liver fibrosis, and necrosis characterized livers from YAPKO and DKO mice. This phenotype was weakened in DKO tissues compared to specimens from YAPKO animals. After depletion of YAP in HCs and BECs, YAP expression was induced in non-parenchymal cells (NPCs) in a cholestasis-independent manner. YAP positivity was detected in subgroups of Kupffer cells (KCs) and endothelial cells (ECs). The secretion of pro-inflammatory chemokines and cytokines such as C-X-C motif chemokine ligand 11 (CXCL11), fms-related receptor tyrosine kinase 3 ligand (FLT3L), and soluble intercellular adhesion molecule-1 (ICAM1) was increased in the serum of YAPKO animals. YAP activation in NPCs could contribute to inflammation via TEA domain transcription factor (TEAD)-dependent transcriptional regulation of secreted factors. Conclusion: YAP inactivation in HCs and BECs causes liver damage, and concomitant TAZ deletion does not enhance but reduces this phenotype. Additionally, we present a new mechanism by which YAP contributes to cell–cell communication originating from NPCs. [ABSTRACT FROM AUTHOR]