40 research outputs found

    Differential sensitivity of target genes to translational repression by miR-17~92

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    MicroRNAs (miRNAs) are thought to exert their functions by modulating the expression of hundreds of target genes and each to a small degree, but it remains unclear how small changes in hundreds of target genes are translated into the specific function of a miRNA. Here, we conducted an integrated analysis of transcriptome and translatome of primary B cells from mutant mice expressing miR-17~92 at three different levels to address this issue. We found that target genes exhibit differential sensitivity to miRNA suppression and that only a small fraction of target genes are actually suppressed by a given concentration of miRNA under physiological conditions. Transgenic expression and deletion of the same miRNA gene regulate largely distinct sets of target genes. miR-17~92 controls target gene expression mainly through translational repression and 5’UTR plays an important role in regulating target gene sensitivity to miRNA suppression. These findings provide molecular insights into a model in which miRNAs exert their specific functions through a small number of key target genesCX is a Pew Scholar in Biomedical Sciences. This study is supported by the PEW Charitable Trusts, Cancer Research Institute, National Institute of Health (R01AI087634, R01AI089854, RC1CA146299, R56AI110403, and R01AI121155 to CX), National Natural Science Foundation of China (31570882 to WHL, 31570883 to NX, 31570911 to GF, 91429301 to JH, 31671428 and 31500665 to YZ), 1000 Young Talents Program of China (K08008 to NX), 100 Talents Program of The Chinese Academy of Sciences (YZ), National Program on Key Basic Research Project of China (2016YFA0501900 to YZ), the Fundamental Research Funds for the Central Universities of China (20720150065 to NX and GF), Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (NRF-2015R1C1A1A01052387 to SGK, NRF-2016R1A4A1010115 to SGK and PHK), and 2016 Research Grant from Kangwon National University (SGK)

    Differential Proteomic Analysis of Mammalian Tissues Using SILAM

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    Differential expression of proteins between tissues underlies organ-specific functions. Under certain pathological conditions, this may also lead to tissue vulnerability. Furthermore, post-translational modifications exist between different cell types and pathological conditions. We employed SILAM (Stable Isotope Labeling in Mammals) combined with mass spectrometry to quantify the proteome between mammalian tissues. Using 15N labeled rat tissue, we quantified 3742 phosphorylated peptides in nuclear extracts from liver and brain tissue. Analysis of the phosphorylation sites revealed tissue specific kinase motifs. Although these tissues are quite different in their composition and function, more than 500 protein identifications were common to both tissues. Specifically, we identified an up-regulation in the brain of the phosphoprotein, ZFHX1B, in which a genetic deletion causes the neurological disorder Mowat–Wilson syndrome. Finally, pathway analysis revealed distinct nuclear pathways enriched in each tissue. Our findings provide a valuable resource as a starting point for further understanding of tissue specific gene regulation and demonstrate SILAM as a useful strategy for the differential proteomic analysis of mammalian tissues

    Two-dimensional DFB laser fabricated on dye-doped hybrid zirconia film by soft lithography

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    A two-dimensional (2D) distributed feedback (DFB) structure is fabricated on dye-doped sol-gel derived hybrid zirconia films by soft lithography. The Q-switched Nd:YAG laser (lambda = 532 nm) is used to pump these structures. The lasing emissions of the gain medium doped with Rhodamine 6G (Rh6G) in two perpendicular directions are shown, and the threshold pump energy is measured.National Natural Science Foundation of China [50802080]; Open Foundation of the State Key Lab of Silicon Materials [SKL2010-12]; Natural Science Foundation of Fujian Province, China [2010J01349

    Abiotic Stresses Intervene with ABA Signaling to Induce Destructive Metabolic Pathways Leading to Death: Premature Leaf Senescence in Plants

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    Abiotic stresses trigger premature leaf senescence by affecting some endogenous factors, which is an important limitation for plant growth and grain yield. Among these endogenous factors that regulate leaf senescence, abscisic acid (ABA) works as a link between the oxidase damage of cellular structure and signal molecules responding to abiotic stress during leaf senescence. Considering the importance of ABA, we collect the latest findings related to ABA biosynthesis, ABA signaling, and its inhibitory effect on chloroplast structure destruction, chlorophyll (Chl) degradation, and photosynthesis reduction. Post-translational changes in leaf senescence end with the exhaustion of nutrients, yellowing of leaves, and death of senescent tissues. In this article, we review the literature on the ABA-inducing leaf senescence mechanism in rice and Arabidopsis starting from ABA synthesis, transport, signaling receptors, and catabolism. We also predict the future outcomes of investigations related to other plants. Before changes in translation occur, ABA signaling that mediates the expression of NYC, bZIP, and WRKY transcription factors (TFs) has been investigated to explain the inducing effect on senescence-associated genes. Various factors related to calcium signaling, reactive oxygen species (ROS) production, and protein degradation are elaborated, and research gaps and potential prospects are presented. Examples of gene mutation conferring the delay or induction of leaf senescence are also described, and they may be helpful in understanding the inhibitory effect of abiotic stresses and effective measures to tolerate, minimize, or resist their inducing effect on leaf senescence

    Distributed feedback leaky laser emission from dye doped gel-glass dispersed liquid crystal thin film patterned by soft lithography

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    National Natural Science Foundation of China [50802080]; State Key Lab of Silicon Materials [SKL2010-12]; Natural Science Foundation of Fujian Province, China [2010J01349]Gel-glass dispersed liquid crystal (GDLC) thin films doped with organic laser dye Rhodamine 6G (R6G) were prepared via a sol-gel procedure of tetraethyl orthosilicate (TEOS) and ethyl triethoxisilane (ETES). As characterized by scanning electronic microscope (SEM), surface-relief structures were successfully patterned on lower refractive index GDLC thin films by soft lithographic technology, which support distributed feedback (DFB) laser emission based on leaky mode propagation. The performance of the DFB laser emission was investigated and the spectral narrowing of the emitted radiation and the fine structure pattern were found to be controlled by the doping concentration of liquid crystal (LC) 4-cyano-4'-pentylbiphenyl (5CB). We also showed the synchronous excitation of a DFB lasing with random lasing mediated by light scattering inside the same GDLC leaky waveguide. (C) 2011 Elsevier B.V. All rights reserved

    Thermo-switchable multi-wavelength laser emission from a dye-doped nematic liquid-crystal device

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    National Natural Science Foundation of China [50802080]; Natural Science Foundation of Fujian Province, China [2010J01349]; Open Foundation Project of the State Key Lab of Silicon Materials [SKL2010-12]A sandwich-type laser device with a surface-relief grating inside was infiltrated with dye-doped nematic liquid-crystals which functioned as gain media. The surface-relief grating was fabricated by soft lithographic technique on a sol-gel derived zirconium-doped hybrid film using a polydimethyl-siloxane replica. The optical properties of the distributed feedback (DFB) resonator were modified by introducing a high refractive index layer consisting of niobium pentoxide subsequently. Thermal induced shift of amplified spontaneous emission spectrum, switching of multi-wavelength DFB laser emission and occurrence of random lasing were demonstrated. (C) 2011 Elsevier B.V. All rights reserved
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