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Effect of open-field experimental warming on the leaf phenology of oriental oak (Quercus variabilis) seedlings

Journal of Plant Ecology 2014年第6期7卷 559-566页

作者： Saerom Han Haegeun Chung Nam Jin Noh sun jeoung lee Wooyong Jo Tae Kyung Yoon Koong Yi Chan-woo Park Suin Ko Yowhan Son Department of Environmental Science and Ecological Engineering Graduate SchoolKorea UniversitySeoul 136-713Korea Department of Environmental Engineering Konkuk UniversitySeoul 143-701Korea River Basin Research Center Gifu UniversityGifu 501-1193Japan Forest and Climate Change Center Korea Forest Research InstituteSeoul 130-712Korea Hanlim Patent and Law Office Seoul 152-050Korea Forest Soil and Water Conservation Division Korea Forest Research InstituteSeoul 130-712Korea Environmental Policy Research Group Korea Environment InstituteSeoul 122-706Korea

Aims An open-field warming experiment enables us to test the effects of projected temperature increase on change in plant phenology with fewer confounding factors and to study phenological response to temperature ranges beyond natural *** study aims to(i)examine the effect of temperature increase on leaf unfold-ing and senescence of oriental oak(Quercus variabilis Blume)under experimental warming and(ii)measure temperature-related parameters used in estimating phenological response to tempera-ture *** Using an open-field warming system with infrared heaters,we increased the air temperature by~3℃ in the warmed plots compared with that of the control plots consistently for 2 *** unfolding and senescence dates of *** seedlings were recorded and temperature-related phenological parameters were *** Findings The timing of leaf unfolding was advanced by 3-8 days(1.1-3.0 days/℃)and the date of leaf senescence was delayed by 14-19 days(5.0-7.3 days/℃)under elevated air ***,the cumulative degree days(CDD)of leaf unfolding were not significantly changed by experimental warming,which suggest the applicability of a constant CDD value to estimate the change in spring leaf phe-nology under 3℃ *** ranges of advancement and temperature sensitivity in spring phenology and delayed autumn phe-nology and proposed temperature parameters from this study might be applied to predict future phenological change.

关键词： climate change cumulative degree days experimental warming leaf senescence leaf unfolding

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Nontarget screening using passive air and water sampling with a level Ⅱ fugacity model to identify unregulated environmental contaminants

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Journal of Environmental Sciences 2017年第12期29卷 84-91页

作者： In-Young Chung Yu-Mi Park Hyun-jeoung lee Hyuk Kim Dong-Hoon Kim Il-Gyu Kim Sang-Min Kim Young-sun Do Kwang-Seol Seok Jung-Hwan Kwon Chemical Research Division Environmental Health Research Department National Institute of Environmental ResearchIncheon Division of Environmental Science and Ecological Engineering Korea University

It is thought that there are many unregulated anthropogenic chemicals in the *** risk assessment of chemicals, it is essential to estimate the predicted environmental concentrations. As an effort of identifying residual organic contaminants in air and water in Korea, nontarget screening using two-dimensional gas chromatography time-of-flight mass spectrometry（GC × GC-TOFMS） was conducted at 10 sites using polyurethane foam passive air sampler and at 6 sites using polydimethyl siloxane（PDMS） passive water sampler in three different seasons in 2014. More than 600 chemical peaks were identified satisfying the identification criteria in air and water samples, respectively, providing a list for further investigation. Chemical substances with reported national emission rates in2014（n = 149） were also screened for potential existence in the environment using a level Ⅱ fugacity model. Most of chemical substances classified as not detectable were not identified with detection frequency greater than 20% by nontarget screening, indicating that a simple equilibrium model has a strong potential to be used to exclude chemicals that are not likely to remain in the environment after emissions from targeted monitoring.

关键词： Nontarget screening GC × GC-TOFMS Passive sampling Pollutant release and transfer register(PRTR) Fugacity model

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Tip60 Tumor Suppressor Requires Its NLS Motif to Interact with Importin <i>α</i>

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CellBio 2019年第1期8卷 1-16页

作者： Eun jeoung lee sung Hwa Shin Sang sun Kang CdmoGen 530 Jikji-daero Heungdeok-gu Cheongju Chungbuk Republic of Korea Department of Biology Education Chungbuk National University Chungdae-ro Seowon-gu Cheongju Chungbuk Republic of Korea

Tip60 is a specific member of MYST (Moz-Ybf2/Sas3-Sas2-Tip60) family of nuclear histone acetyltransferases (HAT). It is essential for cellular survival, differentiation, and metabolism. A putative canonical NLS motif between the chromo domain and the zinc finger of Tip60 was identified. Here we show evidence that Tip60 is associated with importin α as its substrate and transported from cytoplasm to the nucleus. Pull down assay revealed that Tip60 was physically associated with importin α both in vivo and in vitro. Confocal microscopic observation showed that Tip60 and importin α were co-localized with each other. The localization of Tip60 to the nuclear and its interaction with importin α was disrupted when its putative NLS motif for binding to importin α was mutated (219RKRK222 → 219AAAA222). However, attachment of this putative NLS motif to a cytoplasmic protein (YAP 1-210 fragment) promoted its nuclear localization. Based on transient transfection, Tip60 NLS motif mutant showed a substantial reduction in self-acetylation, HAT activity, and apoptotic ability whereas wild type Tip60 did not show such reduction. Taken together, our results demonstrate that importin α transports Tip60 from the cytoplasm to the nucleus through binding to the putative NLS motif of Tip60 for its tumor suppressing function.

关键词： Tip60 Importin α Nuclear Localization Sequence Protein-Protein Interaction HAT Activity Cell Survival

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Phosphorylation on TRPV4 Serine Residue 824 Enhances Its Association with PGM1

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American Journal of Molecular Biology 2016年第1期6卷 33-44页

作者： sung Hwa Shin Eun jeoung lee sunghee Hyun Sang sun Kang Department of Biology Education Chungbuk National University Cheongju Republic of Korea Department of Internal Medicine Chungbuk National University Cheongju Republic of Korea Department of Biomedical Laboratory Science Eulji University Daejeon Republic of Korea

The TRPV4 cation channel is expressed in a broad range of tissues and participates in the generation of a Ca2+ signal and/or depolarization of membrane potential. Here, human phosphoglucomutase- 1 (PGM1), an enzyme that converts glucose-6 phosphate to glucose-1 phosphate in the glycolysis pathway, as the first auxiliary protein of TRPV4 Ca2+ channels, is identified with yeast two hybrid system, coimmunoprecipitation, confocal microscopy, and GST pull-down assays. TRPV4 forms a complex with PGM1 through its C-terminal cytoplasmic domain. Because it is demonstrated that TRPV4 serine residue 824 (S824) is phosphorylated by serum/glucocorticoid regulated kinase 1, we elucidate the effect of TRPV4 S824 phosphorylation on TRPV association with PGM1. Even an inactivated mutant version of TRPV4, S824A, exhibited a decreased ability to bind PGM1, an activated phosphomimetic mutant version of TRPV4, S824D, exhibited enhanced binding to PGM1. Thus, formation of the TRPV4/PGM1 complex and localization of this complex to the plasma membrane appear to be regulated by the phosphorylation status of residue S824 in TRPV4. The newly identified interactor of TRPV4 may help the molecular pathways modulating transport activity or glucose metabolism, respectively.

关键词： Membrane Localization Phosphoglucomutase1 Phosphorylation Protein-Protein Interaction TRPV4

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Ablation of TRPV4 in HepG2 with Its CRISPR/Cas9 Enhances Its Wound Healing

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American Journal of Molecular Biology 2020年第1期10卷 74-89页

作者： Eun jeoung lee sung Hwa Shin sunghee Hyun Sang sun Kang CdmoGen Cheongju Republic of Korea Department of Pre-Medicine School of Medicine Eulji University Daejeon Republic of Korea Department of Biology Education Chungbuk National University Cheongju Republic of Korea

TRPV4 activity modulates cell activities including receptor trafficking and transcriptional or translational regulations. We tested its CRISPR/Cas9 scissor efficacy in HepG2 (HEK293) cell noticed that it worked well in both cell lines to eliminate TRPV4 genome sequences. To confirm TRPV4 functions in the cell morphology maintenance and cell growth (beyond Ca2+ channel), we compared its wound healing, cell surface area, survival property and soft agar growth ability after deletion of TRPV4 gene in the cells with its CRISPR/Cas9 system. With these experiments, we confirmed that TRPV4 is required not only to function as Ca2+ channel but also to maintain its proper cell morphology as a corner stone protein on the cell adhesion junction.

关键词： TRPV4 Ca2+ Ion Channel E-Cadherin Tubulin Soft Agar Growth CRISPR/Cas9 Scissor System

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SGK1 Inhibits ULK2 Autophagy Activity

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American Journal of Molecular Biology 2020年第1期10卷 12-28页

作者： sung Hwa Shin Eun jeoung lee sunghee Hyun Sang sun Kang Department of Biology Education Chungbuk National University Cheongju Korea Department of Biomedical Laboratory Science Eulji University Daejeon Korea

Serum- and glucocorticoid-induced kinase 1 (SGK1) is known to have consensus sequence of phosphorylation site R-x-R-x-x-(S/T)-Φ, where Φ is any hydrophobic amino acid and arginine residues are conserved at positions −5 and −3 relative to positions of Ser/Thr residues that are phosphorylated in the presence of SGK1. UNC-21-like kinase 2 (ULK2) also harbors putative SGK1 phosphorylation sites at both Ser507 (502RsRnsSG508) and Ser750 (745RtRttSV751) residues. Thus, the objective of this study was to determine whether Ser507 and Ser750 residues of ULK2 could be phosphorylation sites of SGK1 as one of its authentic substrate proteins. Using ULK2 507 and 750 serine residue un- or phosphorylation analog (S507AS750A or 507DS750D), we observed that modification of Ser507 or Ser750 residue was required to activate the kinase activity of ULK2 and sensitize ULK2 to stress or starvation while simultaneously enhancing its active state and autophagy characteristics, suggesting that phosphorylation at Ser750 or Ser507 residue could modulate its subcellular localization and protein interaction with AMPK1α to activate ULK2. We also observed that ULK2 autophagy activity was enhanced by GSK650394 (an SGK1 inhibitor) to compensate survival capacity through increasing its association with LC3 and phosphorylation. When SGK1 known to be associated with cell survival was inhibited by GSK650394, ULK2 autophagy pathway was activated to avoid cell death alternatively. Thus, our observations indicate that phosphorylation of ULK2 by SGK1 can regulate cell survival as an alternative modulation of ULK2 functions.

关键词： ULK-2 SGK1 Phosphorylation Autophagy Cell Survival Signal Transduction

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The interaction between Fe65 and Tip60 is regulated by S-nitrosylation on 440 cystein residue of Fe65

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Advances in Biological Chemistry 2011年第3期1卷 109-118页

作者： Eun jeoung lee sung Hwa Shin sunghee Hyun Jaesun Chun Sang sun Kang 不详

The S-Nitrosylation of protein thiol groups by NO is a widely recognized protein modification. The treat-ment of cells with NOBF4 induces the S-nitrosylation of FE65. In this study, we present evidence showing that FE65 modified by NO (Nitric Oxide) via S-nitrosylation induces functional changes in the protein that inhibits the HAT activity of Tip60. The results of mutational analysis of FE65 demonstrated further that the cysteine residue of FE65 (Cys440) is critical to the process of S-nitrosylation. The mutation of the cysteine residue which completely ablated the S-nitrosylation of FE65 also lost its inhibitory effects on Tip60 HAT activity. Thus, our findings show, for the first time, that the novel regulation mechanism of Tip60 activity may operate via FE65 binding, which is enhanced by S-nitrosylation on the FE65 Cys440 residue. This study describes the interaction between FE65 and Tip60, which is enhanced by a posttransla-tional modification of FE65 (through S-nitrosylation) by NO, promoting the association of the FE65-Tip60 protein complex and inhibiting both the HAT activity of Tip60 and cell death.

关键词： S-Nitrosylation NO(Nitric Oxide) FE65 HAT activity Tip60

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