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In light of breakthroughs in superconductivity under high pressure, and considering that record critical temperatures (T_cs) across various systems have been achieved under high pressure, the primary challenge for higher T_cshould no longer solely be to increase T_cunder extreme conditions but also to reduce, or ideally eliminate, the need for applied pressure in retaining pressure-induced or -enhanced superconductivity. The topological semiconductor Bi_0.5Sb_1.5Te₃(BST) was chosen to demonstrate our approach to addressing this challenge and exploring its intriguing physics. Under pressures up to ~50 GPa, three superconducting phases (BST-I, -II, and -III) were observed. A superconducting phase in BST-I appears at ~4 GPa, without a structural transition, suggesting the possible topological nature of this phase. Using the pressure-quench protocol (PQP) recently developed by us, we successfully retained this pressure-induced phase at ambient pressure and revealed the bulk nature of the state. Significantly, this demonstrates recovery of a pressure-quenched sample from a diamond anvil cell at room temperature with the pressure-induced phase retained at ambient pressure. Other superconducting phases were retained in BST-II and -III at ambient pressure and subjected to thermal and temporal stability testing. Superconductivity was also found in BST with T_cup to 10.2 K, the record for this compound series. While PQP maintains superconducting phases in BST at ambient pressure, both depressurization and PQP enhance its T_c, possibly due to microstructures formed during these processes, offering an added avenue to raise T_c. These findings are supported by our density-functional theory calculations. 

Arabidopsis RESISTANCE TO POWDERY MILDEW 8.2 (RPW8.2) is specifically induced by the powdery mildew (PM) fungus (Golovinomyces cichoracearum) in the infected epidermal cells to activate immunity. However, the mechanism of RPW8.2-induction is not well understood. Here, we identify a G. cichoracearum effector that interacts with RPW8.2, named Gc-RPW8.2 interacting protein 1 (GcR8IP1), by a yeast two-hybrid screen of an Arabidopsis cDNA library. GcR8IP1 physically associated with RPW8.2 with its RING finger domain that is essential and sufficient for the association. GcR8IP1 was secreted and translocated into the nucleus of host cell infected with PM. Association of GcR8IP1 with RPW8.2 led to an increase of RPW8.2 in the nucleus. In turn, the nucleus-localised RPW8.2 promoted the activity of the RPW8.2 promoter, resulting in transcriptional self-amplification of RPW8.2 to boost immunity at infection sites. Additionally, ectopic expression or host-induced gene silencing of GcR8IP1 supported its role as a virulence factor in PM. Altogether, our results reveal a mechanism of RPW8.2-dependent defense strengthening via altered partitioning of RPW8.2 and transcriptional self-amplification triggered by a PM fungal effector, which exemplifies an atypical form of effector-triggered immunity.