Non-damaging ultraviolet B (UV-B) light promotes photomorphogenic development and stress acclimation through UV-B-specific signal transduction in Arabidopsis. UV-B irradiation induces monomerization and nuclear translocation of the UV-B photoreceptor UV RESISTANCE LOCUS 8 (UVR8). However, it is not clear how the nuclear localization of UVR8 leads to changes in global gene expression. Here, we reveal that nuclear UVR8 governs UV-B-responsive transcriptional networks in concert with several previously known transcription factors, including ELONGATED HYPOCOTYL 5 (HY5) and PHYTOCHROME INTERACTING FACTOR 4 (PIF4). Based on the transcriptomic analysis, we identify MYB13 as a novel positive regulator in UV-B-induced cotyledon expansion and stress acclimation. MYB13 is UV-B inducible and is predominantly expressed in the cotyledons. Our results demonstrate that MYB13 protein functions as a transcription factor to regulate the expression of genes involved in auxin response and flavonoid biosynthesis through direct binding with their promoters. In addition, photoactivated UVR8 interacts with MYB13 in a UV-B-dependent manner and differentially modulates the affinity of MYB13 with its targets. Taken together, our results elucidate the cooperative function of the UV-B photoreceptor UVR8 with various transcription factors in the nucleus to orchestrate the expression of specific sets of downstream genes and, ultimately, mediate plant responses to UV-B light.

Photomorphogenesis is a pivotal developmental strategy used by plants to respond to environmental light levels. During emergence from the soil and the establishment of photomorphogenesis, seedlings encounter increasing levels of UV-B irradiation and develop adaptive responses accordingly. However, the molecular mechanisms that orchestrate UV-B signaling cascades remain elusive. Here, we provide biochemical and genetic evidence that the prolonged signaling circuits of UV-B–induced photomorphogenesis involve two sets of E3 ligases and a transcription factor inArabidopsis thaliana. The UV-B–inducible protein RUP1/RUP2 associates with the CUL4-DDB1 scaffold to form an E3 ligase, which represses photomorphogenesis by mediating the degradation of HY5, the hub transcription factor in the light signaling pathway. Conversely, COP1 directly targets RUP1/RUP2 for ubiquitination and degradation, leading to balanced RUP1/RUP2 accumulation, alleviation of the COP1–HY5 interaction, and stabilization of HY5 protein. Therefore, our study reveals that these two E3-substrate modules, CUL4-DDB1-RUP1/RUP2-HY5 and COP1-RUP1/RUP2, constitute the repression and derepression machinery by which plants respond to prolonged UV-B irradiation in photomorphogenic development.

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Ferrimagnetic insulators (FMIs) have abundant advantages for the application in spintronic devices, which have attracted intensive studies. However, in most previous studies on heavy metal (HM)/FMI bilayers, the FMI layers are deposited by pulsed laser deposition (PLD), and the HM layers are deposited by magnetron sputtering. This will cause the interfacial contamination due to the inevitable vacuum breaking, and then significantly affect the spin‐orbit torque (SOT) generation and the Dzyaloshinskii–Moriya interaction (DMI) in the HM/FMI bilayers. In this work, the SOT and DMI in the HM/FMI bilayers deposited by magnetron sputtering without vacuum breaking are studied. The successful fabrication of the Tm3Fe5O12 (TmIG) layer, a typical FMI, with good crystallinity and perpendicular magnetic anisotropy (PMA) by magnetron sputtering is first demonstrated. Then by systematically varying the TmIG thickness, the SOT and DMI in the Pt/TmIG bilayers are studied. It is shown that the effective spin Hall angle in the Pt/TmIG bilayers is much larger than most previously reported values. It is further demonstrated that the DMI constant scales linearly with the inverse of the TmIG thickness, indicating the interfacial origin of the DMI. The study provides a piece of information for the basic understandings of the SOT and DMI in the HM/FMI bilayers.

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Mn2+ ions doped ZnS semiconductor nanocrystals (ZnS:Mn NCs) were synthesized using colloidal chemical method at 70 degrees C without any capping agents. The as-prepared undoped ZnS and ZnS:Mn NCs were characterized by UV-Vis absorption spectra, fluorescent emission spectra, X-ray powder diffraction (XRD), inductively coupled plasma analysis (ICP), X-ray photoelectron spectroscopy (XPS), Dynamic light scattering (DLS), cyclic voltammogram and electronic transmission microscopy (TEM). The dependence of photoluminescence of ZnS:Mn NCs on dopant concentration was studied. The results show that Mn2+ ions mainly stay at ZnS nanocystal surface, and Mn2+-surface defect state complex was formed, as a result of which, surface defect emission of ZnS nanocrystals was substituted with Mn2+-related PL emission. The strongest fluorescent emission intensity was obtain at 1.85 at% Mn2+ doped ZnS:Mn NCs. The Mn2+ doped ZnS:Mn NCs are of 5 nm in diameter. The emission peak at 575 nm is attributed to d-d (4T1 --> 6A1) transition of Mn2+ ions. The existence of Mn2+-related photoluminescence could be well correlated with cyclic voltammogram of Mn2+-doped NCs, where pair of oxidation and reduction peaks were clearly observed due to the doped Mn2+ ions. The adsorbed Mn2+ ions on ZnS NCs produced neither Mn2+ emission nor redox peaks. For heavily doped ZnS:Mn NCs (4.87 at%), redox peaks gap in cyclic voltammogram became larger and new oxidation peak appeared. Correspondingly, when the Mn2+ doping concentration reached 4.87 at%, the Mn2+-related emission totally disappears due to the Mn-Mn interactions. This work implys that electrochemical technique is possibly an useful tool to probe the local structure of doped Mn2+ ions.