Photoperiodic flowering is one of the most important pathways to govern flowering in rice (Oryza sativa), in which Heading date 1 (Hd1), an ortholog of the Arabidopsis CONSTANS gene, encodes a pivotal regulator. Hd1 promotes flowering under short-day conditions (SD) but represses flowering under long-day conditions (LD) by regulating the expression of Heading date 3a (Hd3a), the FLOWERING LOCUS T (FT) ortholog in rice. However, the molecular mechanism of how Hd1 changes its regulatory activity in response to day length remains largely unknown. In this study, we demonstrated that the repression of flowering in LD by Hd1 is dependent on the transcription factor DAYS TO HEADING 8 (DTH8). Loss of DTH8 function results in the activation of Hd3a by Hd1, leading to early flowering. We found that Hd1 directly interacts with DTH8 and that the formation of the DTH8-Hd1 complex is necessary for the transcriptional repression of Hd3a by Hd1 in LD, implicating that the switch of Hd1 function is mediated by DTH8 in LD rather than in SD. Furthermore, we revealed that DTH8 associates with the Hd3a promoter to modulate the level of H3K27 trimethylation (H3K27me3) at the Hd3a locus. In the presence of the DTH8-Hd1 complex, the H3K27me3 level was increased at Hd3a, whereas loss of DTH8 function resulted in decreased H3K27me3 level at Hd3a. Taken together, our findings indicate that, in response to day length, DTH8 plays a critical role in mediating the transcriptional regulation of Hd3a by Hd1 through the DTH8-Hd1 module to shape epigenetic modifications in photoperiodic flowering.

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.

Expression of the CFTR protein is thought to be physiologically important only in exocrine epithelial cells. However, chronic respiratory inflammation and infection remain unexplained phenomena in disease pathogenesis. Non‐transformed, antigen‐responsive CD4+ T cells cloned from healthy controls and CF patients homozygous or heterozygous for the δF508 mutation transcribed CFTR mRNA and expressed immunoreactive cytoplasmic CFTR protein. T cell clones (TCC) from controls and CF patients displayed equivalent Ca2+‐mediated Cl− current; however, TCC from patients with CF but not controls displayed defective cAMP‐mediated Cl− current. Although CF‐derived TCC preserved mitogen and antigen proliferative responses and specificity to tetanus toxoid epitopes, they selectively secreted ≈ 45% less IL‐10 compared with control TCC after activation with concanavalin A (Con A) (624 ± 101 versus 1564 ± 401 pg/ml per 106 cells, respectively; P = 0.04) or anti‐CD3/phorbol ester (5148 ± 1634 versus 11 788 ± 2390 pg/ml; P = 0.05). This difference was independent of atopy. Secretion of interferon‐gamma, IL‐2, and IL‐4 was comparable in CF and control TCC after both forms of activation, while IL‐5 was reduced in CF TCC following anti‐CD3/phorbol myristate acetate (PMA) but not after Con A. We conclude that expression of mutant CFTR in human TCC is accompanied by ion channel dysfunction characteristic of the CF phenotype, and is accompanied by a reduction in IL‐10 secretion after polyclonal activation. It is possible that disruption of IL‐10‐mediated anti‐inflammatory homeostasis may contribute to early onset sustained inflammation in CF airways.

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Many researches on polar-molecular electrorheological (PMER) fluids with giant electrorheological effects were reported in recent years. The particles of PMER fluids (PMER particles) are known to have a dielectric core with high dielectric constant and a shell of polar molecules. Our calculation of local electric fields using the finite element approach shows that the local electric field can cause an orientational polarization of the polar molecules. The saturation of the orientational polarization occurs on the outer shells of two nearby PMER particles. Then, it causes the strong outer shell-outer shell interaction between the two particles, and this kind of interaction is just responsible for the giant electrorheological effect. It is further realized that the PMER effect is mainly due to the interaction of the tail-head connected polar molecules within the two outer shells between the two PMER particles. Our theoretical results of static yield stresses are shown to be in excellent agreement with the reported experimental data by several groups. For general PMER fluids, the calculated static yield stress is nearly proportional to R x-1 . When h/R, the ratio between the thickness of shells and radius of PMER particles, changes from 0.05 to 0.5, the index x changes accordingly from 0.64 to 0.51. It is also found that particles with thinner thickness h and smaller radius R have larger electrorheological effects until the static yield stress shows a peak when R reaches about 10 nm.

Municipal mergers have become a worldwide phenomenon in the past few decades, primarily advanced to exploit economies of scale. While most evaluations of municipal mergers have focused on the efficiency of local public goods provision, it is rare in the literature to explore how such mergers promote economic growth in a developing country context. This research investigates the economic consequences of a policy experiment of city-county mergers (che xian she qu) in China during the period 2000-2004. Using comprehensive datasets at city, county and firm levels, we present evidence that the merger significantly increases local economic development, and the magnitude of the effect depends on local endowments related to agglomeration forces. The results are robust to a number of different model specifications. We further verify that improved transport infrastructure and urban agglomeration economies after merger are potential contributors to the positive merger effects.JEL classifications: R1, R5, H11, O18.

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