Academia Sinica

About: Academia Sinica is a facility organization based out in Taipei, Taiwan. It is known for research contribution in the topics: Population & Gene. The organization has 52086 authors who have published 65998 publications receiving 1728114 citations. The organization is also known as: Central Research Academy.

Giant and anisotropic many-body spin–orbit tunability in a strongly correlated kagome magnet

Abstract: Owing to the unusual geometry of kagome lattices—lattices made of corner-sharing triangles—their electrons are useful for studying the physics of frustrated, correlated and topological quantum electronic states1–9. In the presence of strong spin–orbit coupling, the magnetic and electronic structures of kagome lattices are further entangled, which can lead to hitherto unknown spin–orbit phenomena. Here we use a combination of vector-magnetic-field capability and scanning tunnelling microscopy to elucidate the spin–orbit nature of the kagome ferromagnet Fe3Sn2 and explore the associated exotic correlated phenomena. We discover that a many-body electronic state from the kagome lattice couples strongly to the vector field with three-dimensional anisotropy, exhibiting a magnetization-driven giant nematic (two-fold-symmetric) energy shift. Probing the fermionic quasi-particle interference reveals consistent spontaneous nematicity—a clear indication of electron correlation—and vector magnetization is capable of altering this state, thus controlling the many-body electronic symmetry. These spin-driven giant electronic responses go well beyond Zeeman physics and point to the realization of an underlying correlated magnetic topological phase. The tunability of this kagome magnet reveals a strong interplay between an externally applied field, electronic excitations and nematicity, providing new ways of controlling spin–orbit properties and exploring emergent phenomena in topological or quantum materials10–12. The topological magnet Fe3Sn2 exhibits a giant nematic energy shift of a many-body electronic state, demonstrating anisotropic spin–orbit tunability.

EGFR Promotes Lung Tumorigenesis by Activating miR-7 through a Ras/ERK/Myc Pathway That Targets the Ets2 Transcriptional Repressor ERF

Abstract: MicroRNAs (miRNA) mediate distinct gene regulatory pathways triggered by epidermal growth factor receptor (EGFR) activation, which occurs commonly in lung cancers with poor prognosis. In this study, we report the discovery and mechanistic characterization of the miRNA miR-7 as an oncogenic "oncomiR" and its role as a key mediator of EGFR signaling in lung cancer cells. EGFR activation or ectopic expression of Ras as well as c-Myc stimulated miR-7 expression in an extracellular signal-regulated kinase (ERK)-dependent manner, suggesting that EGFR induces miR-7 expression through a Ras/ERK/Myc pathway. In support of this likelihood, c-Myc bound to the miR-7 promoter and enhanced its activity. Ectopic miR-7 promoted cell growth and tumor formation in lung cancer cells, significantly increasing the mortality of nude mice hosts, which were orthotopically implanted with lung cancers. Quantitative proteomic analysis revealed that miR-7 decreased levels of the Ets2 transcriptional repression factor ERF, the coding sequence of which was found to contain a miR-7 complementary sequence. Indeed, ectopic miR-7 inhibited production of ERF messages with a wild-type but not a silently mutated coding sequence, and ectopic miR-7 rescued growth arrest produced by wild-type but not mutated ERF. Together, these results identified that ERF is a direct target of miR-7 in lung cancer. Our findings suggest that miR-7 may act as an important modulator of EGFR-mediated oncogenesis, with potential applications as a novel prognostic biomarker and therapeutic target in lung cancer.

NITROGEN LIMITATION ADAPTATION, a Target of MicroRNA827, Mediates Degradation of Plasma Membrane–Localized Phosphate Transporters to Maintain Phosphate Homeostasis in Arabidopsis

Abstract: Members of the Arabidopsis thaliana PHOSPHATE TRANSPORTER1 (PHT1) family are key players in acquisition of Pi from the rhizosphere, and their regulation is indispensable for the maintenance of cellular Pi homeostasis. Here, we reveal posttranslational regulation of Pi transport through modulation of degradation of PHT1 proteins by the RING-type ubiquitin E3 ligase, NITROGEN LIMITATION ADAPTATION (NLA). Loss of function of NLA caused high Pi accumulation resulting from increases in the levels of several PHT1s at the protein rather than the transcript level. Evidence of decreased endocytosis and ubiquitination of PHT1s in nla mutants and interaction between NLA and PHT1s in the plasma membranes suggests that NLA directs the ubiquitination of plasma membrane–localized PHT1s, which triggers clathrin-dependent endocytosis followed by endosomal sorting to vacuoles. Furthermore, different subcellular localization of NLA and PHOSPHATE2 (PHO2; a ubiquitin E2 conjugase) and the synergistic effect of the accumulation of PHT1s and Pi in nla pho2 mutants suggest that they function independently but cooperatively to regulate PHT1 protein amounts. Intriguingly, NLA and PHO2 are the targets of two Pi starvation-induced microRNAs, miR827 and miR399, respectively. Therefore, our findings uncover modulation of Pi transport activity in response to Pi availability through the integration of a microRNA-mediated posttranscriptional pathway and a ubiquitin-mediated posttranslational regulatory pathway.