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- 발행기관 : The Company of Biologists Limited (검색결과 31 건)
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Hwang, Young Sun,Seo, Minseok,Lee, Bo Ram,Lee, Hong Jo,Park, Young Hyun,Kim, Sang Kyung,Lee, Hyung Chul,Choi, Hee Jung,Yoon, Joon,Kim, Heebal,Han, Jae Yong The Company of Biologists Limited 2018 Development (Cambridge) Vol.145 No.6
<P>The phylogenomics and comparative functional genomics of avian species were investigated in the Bird 10,000 Genomes (B10K) project because of the important evolutionary position of birds and their value as a research model. However, the systematic profiling of transcriptional changes prior to oviposition has not been investigated in avian species because of the practical difficulties in obtaining pre-oviposited eggs. In this study, a total of 137 pre-oviposited embryos were collected from hen ovaries and oviducts and subjected to RNA-sequencing analyses. Two waves of chicken zygotic genome activation (ZGA) were observed. Functionally distinct developmental programs involving Notch, MAPK, Wnt and TGF beta signaling were separately detected during cleavage and area pellucida formation. Furthermore, the early stages of chicken development were compared with the human and mouse counterparts, highlighting chicken-specific signaling pathways and gradually analogous gene expression via ZGA. These findings provide a genome-wide understanding of avian embryogenesis and comparisons among amniotes.</P>
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Conversion of genomic imprinting by reprogramming and redifferentiation
Kim, Min Jung,Choi, Hyun Woo,Jang, Hyo Jin,Chung, Hyung Min,Arauzo-Bravo, Marcos J.,Schö,ler, Hans R.,Do, Jeong Tae The Company of Biologists Limited 2013 Journal of cell science Vol.126 No.11
<P>Induced pluripotent stem cells (iPSCs), generated from somatic cells by overexpression of transcription factors Oct4, Sox2, Klf4 and c-Myc have the same characteristics as pluripotent embryonic stem cells (ESCs). iPSCs reprogrammed from differentiated cells undergo epigenetic modification during reprogramming, and ultimately acquire a similar epigenetic state to that of ESCs. In this study, these epigenetic changes were observed in reprogramming of uniparental parthenogenetic somatic cells. The parthenogenetic pattern of imprinted genes changes during the generation of parthenogenetic maternal iPSCs (miPSCs), a process referred to as pluripotent reprogramming. We determined whether altered imprinted genes are maintained or revert to the parthenogenetic state when the reprogrammed cells are redifferentiated into specialized cell types. To address this question, we redifferentiated miPSCs into neural stem cells (miPS-NSCs) and compared them with biparental female NSCs (fNSCs) and parthenogenetic NSCs (pNSCs). We found that pluripotent reprogramming of parthenogenetic somatic cells could reset parthenogenetic DNA methylation patterns in imprinted genes, and that alterations in DNA methylation were maintained even after miPSCs were redifferentiated into miPS-NSCs. Notably, maternally methylated imprinted genes (<I>Peg1</I>, <I>Peg3</I>, <I>Igf2r</I>, <I>Snrpn</I> and <I>Ndn</I>), whose differentially methylated regions were fully methylated in pNSCs, were demethylated and their expression levels were found to be close to the levels in normal biparental fNSCs after reprogramming and redifferentiation. Our findings suggest that pluripotent reprogramming of parthenogenetic somatic cells followed by redifferentiation leads to changes in DNA methylation of imprinted genes and the reestablishment of gene expression levels to those of normal biparental cells.</P>
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Woo, Hye Ryun,Kim, Hyo Jung,Nam, Hong Gil,Lim, Pyung Ok The Company of Biologists Limited 2013 Journal of cell science Vol.126 No.21
<P>How do organisms, organs, tissues and cells change their fate when they age towards senescence and death? Plant leaves provide a unique window to explore this question because they show reproducible life history and are readily accessible for experimental assays. Throughout their lifespan, leaves undergo a series of developmental, physiological and metabolic transitions that culminate in senescence and death. Leaf senescence is an ‘altruistic death’ that allows for the degradation of the nutrients that are produced during the growth phase of the leaf and their redistribution to developing seeds or other parts of the plant, and thus is a strategy that has evolved to maximize the fitness of the plant. During the past decade, there has been significant progress towards understanding the key molecular principles of leaf senescence using genetic and molecular studies, as well as ‘omics’ analyses. It is now apparent that leaf senescence is a highly complex genetic program that is tightly controlled by multiple layers of regulation, including at the level of chromatin and transcription, as well as by post-transcriptional, translational and post-translational regulation. This Commentary discusses the latest understandings and insights into the underlying molecular mechanisms, and presents the perspectives necessary to enable our system-level understanding of leaf senescence, together with their possible implications for aging in general.</P>
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Song, Yoo Sung,Lee, Hye-Jin,Prosselkov, Pavel,Itohara, Shigeyoshi,Kim, Eunjoon The Company of Biologists Limited 2013 Journal of cell science Vol.126 No.21
<P>The initial contact between axons and dendrites at early neuronal synapses is mediated by surface adhesion molecules and is thought to induce synaptic maturation through the recruitment of additional synaptic proteins. The initiation of synaptic maturation should be tightly regulated to ensure that synaptic maturation occurs selectively at subcellular sites of axo-dendritic adhesion. However, the underlying mechanism is poorly understood. Here, we report that the initial trans-synaptic adhesion mediated by presynaptic netrin-G1 and postsynaptic NGL-1 (netrin-G1 ligand-1) induces a cis interaction between netrin-G1 and the receptor protein tyrosine phosphatase LAR (leukocyte antigen-related), and that this promotes presynaptic differentiation. We propose that trans-synaptic adhesions at early neuronal synapses trigger recruitment of neighboring adhesion molecules in a cis manner in order to couple initial axo-dendritic adhesion with synaptic differentiation.</P>
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SNX14 is a bifunctional negative regulator for neuronal 5‐HT<sub>6</sub> receptor signaling
Ha, Chang Man,Park, Daehun,Kim, Yoonju,Na, Myeongsu,Panda, Surabhi,Won, Sehoon,Kim, Hyun,Ryu, Hoon,Park, Zee Yong,Rasenick, Mark M.,Chang, Sunghoe The Company of Biologists Limited 2015 Journal of cell science Vol.128 No.9
<P>The 5-hydroxytryptamine (5-HT, also known as serotonin) subtype 6 receptor (5-HT6R, also known as HTR6) plays roles in cognition, anxiety and learning and memory disorders, yet new details concerning its regulation remain poorly understood. In this study, we found that 5-HT6R directly interacted with SNX14 and that this interaction dramatically increased internalization and degradation of 5-HT6R. Knockdown of endogenous SNX14 had the opposite effect. SNX14 is highly expressed in the brain and contains a putative regulator of G-protein signaling (RGS) domain. Although its RGS domain was found to be non-functional as a GTPase activator for Gas, we found that it specifically bound to and sequestered Gas, thus inhibiting downstream cAMP production. We further found that protein kinase A (PKA)-mediated phosphorylation of SNX14 inhibited its binding to Gas and diverted SNX14 from Gas binding to 5-HT6R binding, thus facilitating the endocytic degradation of the receptor. Therefore, our results suggest that SNX14 is a dual endogenous negative regulator in 5-HT6R-mediated signaling pathway, modulating both signaling and trafficking of 5-HT6R.</P>
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Cdc25A activity is required for the metaphase II arrest in mouse oocytes
Oh, Jeong Su,Susor, Andrej,Schindler, Karen,Schultz, Richard M.,Conti, Marco The Company of Biologists Limited 2013 Journal of cell science Vol.126 No.5
<P>Mammalian oocytes are arrested in metaphase of second meiosis (MII) until fertilization. This arrest is enforced by the cytostatic factor (CSF), which maintains the M-phase promoting factor (MPF) in a highly active state. Although the continuous synthesis and degradation of cyclin B to maintain the CSF-mediated MII arrest is well established, it is unknown whether cyclin-dependent kinase 1 (Cdk1) phosphorylations are involved in this arrest in mouse oocytes. Here, we show that a dynamic equilibrium of Cdk1 phosphorylation is required to maintain MII arrest. When the Cdc25A phosphatase is downregulated, mouse oocytes are released from MII arrest and MPF becomes inactivated. This inactivation occurs in the absence of cyclin B degradation and is dependent on Wee1B-mediated phosphorylation of Cdk1. Thus, our data demonstrate that Cdk1 activity is maintained during MII arrest not only by cyclin turnover but also by steady state phosphorylation.</P>
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Oh, Jun-Young,Kwon, Ara,Jo, Anna,Kim, Hoon,Goo, Yong-Sook,Lee, Jin-A,Kim, Hyong Kyu The Company of Biologists Limited 2013 Journal of cell science Vol.126 No.9
<P>In neurons, transport of a subset of mRNAs to subcellular regions and their translation has a role in synaptic plasticity. Recent studies have suggested a control mechanism of this local translation through mRNA compartmentalization or degradation. Here we report that processing bodies (P-bodies), which are involved in mRNA degradation or storage, are transported to dendrites by conventional kinesin (KIF5A) as a motor protein. Neuronal activation induced by depolarization increased the colocalization of P-bodies with PSD-95 in dendrites. This neuronal activity increased the release of <I>Nd1</I> and <I>Arp2</I> mRNA from the P-bodies and, consequently, reversed the decrease of F-actin (induced by overexpression of Dcp1a) in the dendrites. Our data suggest that the activity-induced redistribution of P-bodies and mRNA release from P-bodies might have a role in synaptic structural plasticity by altering levels of mRNAs that are involved in the dynamics of the actin cytoskeleton in dendrites.</P>
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Lee, Ha-Na,Kundu, Joydeb Kumar,Cha, Young-Nam,Surh, Young-Joon The Company of Biologists Limited 2013 Journal of cell science Vol.126 No.17
<P>Phagocytosis of apoptotic neutrophils, termed efferocytosis, is essential for the resolution of inflammation as it prevents the tissues surrounding the inflamed site from being exposed to the toxic contents of lytic cells. Resolvin D1 (RvD1), endogenously generated from docosahexaenoic acid during resolution of inflammation, is known to stimulate efferocytosis. However, the molecular mechanism underlying RvD1-mediated enhancement of efferocytosis remains largely unresolved. In the present study, murine macrophage-like RAW264.7 cells treated with lipopolysaccharide (LPS) exhibited markedly reduced efferocytic activity, but this was restored by co-incubation with RvD1. RvD1-induced restoration of the efferocytic activity appears to be mediated by downregulation of LPS-induced TNF-α expression. The inhibitory effect of RvD1 on LPS-induced TNF-α expression was associated with enhanced nuclear localization of p50/p50 homodimer and concomitant reduction of p65/p50 heterodimer accumulation in the nucleus. RvD1 triggered phosphorylation and proteasomal degradation of nuclear factor κB1 (NF-κB1) p105 to generate p50, which was subsequently translocated to the nucleus as a p50/p50 homodimer. Knockdown of NF-κB p50 abolished the ability of RvD1 to suppress TNF-α expression and also to restore efferocytosis, suggesting that the replacement of p65/p50 with p50/p50 homodimer in the nucleus is crucial for RvD1-mediated stimulation of efferocytosis. In a murine peritonitis model, intraperitoneal administration of RvD1 abolished the zymosan-A-induced TNF-α production, thereby stimulating efferocytosis. Taken together, these findings indicate that RvD1 expedites resolution of inflammation through induction of efferocytosis by p50/p50-homodimer-mediated repression of TNF-α production.</P>
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Park, Jong-Chan,Jeong, Woo-Jeong,Kim, Mi-Yeon,Min, DoSik,Choi, Kang-Yell The Company of Biologists Limited 2016 Journal of cell science Vol.129 No.15
<P>Ras signaling is tightly regulated during neural stem cell (NSC) differentiation, and defects in this pathway result in aberrant brain development. However, the mechanism regulating Ras signaling during NSC differentiation was unknown. Here, we show that stabilized HRas specifically induces neuronal differentiation of NSCs. Lentivirus-mediated HRas overexpression and knockdown resulted in stimulation and inhibition, respectively, of NSC differentiation into neuron in the ex vivo embryo. Retinoic acid, an active metabolite of vitamin A, promoted neuronal differentiation of NSCs by stabilizing HRas, and HRas knockdown blocked the retinoic acid effect. Vitamin-A-deficient mice displayed abnormal brain development with reduced HRas levels and a reduced thickness of the postmitotic region containing differentiated neurons. All of these abnormal phenotypes were rescued with the restoration of HRas protein levels achieved upon feeding with a retinoic-acid-supplemented diet. In summary, this study shows that retinoic acid stabilizes HRas protein during neurogenesis, and that this is required for NSC differentiation into neurons and murine brain development.</P>
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