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  • 1
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    Enhanced striatal cholinergic neuronal activity mediates l-DOPA-induced dyskinesia in parkinsonian mice [Neuroscience] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-01-12
    Description: Treatment of Parkinson disease (PD) with l-3,4-dihydroxyphenylalanine (l-DOPA) dramatically relieves associated motor deficits, but l-DOPA–induced dyskinesias (LID) limit the therapeutic benefit over time. Previous investigations have noted changes in striatal medium spiny neurons, including abnormal activation of extracellular signal-regulated kinase1/2 (ERK). Using two PD models, the traditional 6-hydroxydopamine toxic lesion and a genetic model with nigrostriatal dopaminergic deficits, we found that acute dopamine challenge induces ERK activation in medium spiny neurons in denervated striatum. After repeated l-DOPA treatment, however, ERK activation diminishes in medium spiny neurons and increases in striatal cholinergic interneurons. ERK activation leads to enhanced basal firing rate and stronger excitatory responses to dopamine in striatal cholinergic neurons. Pharmacological blockers of ERK activation inhibit l-DOPA–induced changes in ERK phosphorylation, neuronal excitability, and the behavioral manifestation of LID. In addition, a muscarinic receptor antagonist reduces LID. These data indicate that increased dopamine sensitivity of striatal cholinergic neurons contributes to the expression of LID, which suggests novel therapeutic targets for LID.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    RNA polymerase IV functions in paramutation in Zea mays (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-03
    Description: Plants have distinct RNA polymerase complexes (Pol IV and Pol V) with largely unknown roles in maintaining small RNA-associated gene silencing. Curiously, the eudicot Arabidopsis thaliana is not affected when either function is lost. By use of mutation selection and positional cloning, we showed that the largest subunit of the presumed maize Pol IV is involved in paramutation, an inherited epigenetic change facilitated by an interaction between two alleles, as well as normal maize development. Bioinformatics analyses and nuclear run-on transcription assays indicate that Pol IV does not engage in the efficient RNA synthesis typical of the three major eukaryotic DNA-dependent RNA polymerases. These results indicate that Pol IV employs abnormal RNA polymerase activities to achieve genome-wide silencing and that its absence affects both maize development and heritable epigenetic changes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erhard, Karl F Jr -- Stonaker, Jennifer L -- Parkinson, Susan E -- Lim, Jana P -- Hale, Christopher J -- Hollick, Jay B -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1201-5. doi: 10.1126/science.1164508.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant and Microbial Biology, 111 Koshland Hall, University of California, Berkeley, CA 94720-3102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251626" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Computational Biology ; DNA-Directed RNA Polymerases/chemistry/genetics/*metabolism ; *Epigenesis, Genetic ; Gene Silencing ; Genes, Plant ; Molecular Sequence Data ; *Mutation ; Phylogeny ; Protein Subunits/chemistry/genetics/metabolism ; RNA, Plant/genetics/metabolism ; RNA, Small Interfering/genetics/metabolism ; Transcription, Genetic ; Zea mays/*enzymology/*genetics/growth & development
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Prkcz null mice show normal learning and memory (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-01-04
    Description: Protein kinase M-zeta (PKM-zeta) is a constitutively active form of atypical protein kinase C that is exclusively expressed in the brain and implicated in the maintenance of long-term memory. Most studies that support a role for PKM-zeta in memory maintenance have used pharmacological PKM-zeta inhibitors such as the myristoylated zeta inhibitory peptide (ZIP) or chelerythrine. Here we use a genetic approach and target exon 9 of the Prkcz gene to generate mice that lack both protein kinase C-zeta (PKC-zeta) and PKM-zeta (Prkcz(-/-) mice). Prkcz(-/-) mice showed normal behaviour in a cage environment and in baseline tests of motor function and sensory perception, but displayed reduced anxiety-like behaviour. Notably, Prkcz(-/-) mice did not show deficits in learning or memory in tests of cued fear conditioning, novel object recognition, object location recognition, conditioned place preference for cocaine, or motor learning, when compared with wild-type littermates. ZIP injection into the nucleus accumbens reduced expression of cocaine-conditioned place preference in Prkcz(-/-) mice. In vitro, ZIP and scrambled ZIP inhibited PKM-zeta, PKC-iota and PKC-zeta with similar inhibition constant (K(i)) values. Chelerythrine was a weak inhibitor of PKM-zeta (K(i) = 76 muM). Our findings show that absence of PKM-zeta does not impair learning and memory in mice, and that ZIP can erase reward memory even when PKM-zeta is not present.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548047/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548047/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Anna M -- Kanter, Benjamin R -- Wang, Dan -- Lim, Jana P -- Zou, Mimi E -- Qiu, Chichen -- McMahon, Thomas -- Dadgar, Jahan -- Fischbach-Weiss, Sarah C -- Messing, Robert O -- AA017072/AA/NIAAA NIH HHS/ -- P50 AA017072/AA/NIAAA NIH HHS/ -- T32 GM007618/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2013 Jan 17;493(7432):416-9. doi: 10.1038/nature11803. Epub 2013 Jan 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ernest Gallo Clinic and Research Center, Department of Neurology, University of California, San Francisco, 5858 Horton Street, Suite 200, Emeryville, California 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23283171" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/genetics ; Behavior, Animal ; Benzophenanthridines/pharmacology ; Cocaine ; Conditioning, Classical ; Cues ; Exons/genetics ; Fear ; Female ; *Gene Deletion ; Male ; Memory/*physiology ; Mice ; Protein Kinase C/analysis/*deficiency/*genetics/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-10-21
    Description: Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendants. The histone H3 lysine 4 trimethylation (H3K4me3) complex, composed of ASH-2, WDR-5 and the histone methyltransferase SET-2, regulates Caenorhabditis elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5 or SET-2 in the parental generation extend the lifespan of descendants up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendants. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendants.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368121/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368121/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greer, Eric L -- Maures, Travis J -- Ucar, Duygu -- Hauswirth, Anna G -- Mancini, Elena -- Lim, Jana P -- Benayoun, Berenice A -- Shi, Yang -- Brunet, Anne -- ARRA-AG31198/AG/NIA NIH HHS/ -- F32-AG037254/AG/NIA NIH HHS/ -- R01 AG031198/AG/NIA NIH HHS/ -- R01-AG31198/AG/NIA NIH HHS/ -- R01-GM058012/GM/NIGMS NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- T32-CA009361/CA/NCI NIH HHS/ -- T32-MH020016/MH/NIMH NIH HHS/ -- England -- Nature. 2011 Oct 19;479(7373):365-71. doi: 10.1038/nature10572.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University, 300 Pasteur Drive, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22012258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/metabolism ; Chromatin/metabolism ; Epigenesis, Genetic/*genetics ; Female ; Gene Expression Regulation ; Gene Knockdown Techniques ; Histone Demethylases/genetics/metabolism ; Histone-Lysine N-Methyltransferase/deficiency/genetics/metabolism ; Histones ; *Inheritance Patterns ; Longevity/*genetics/physiology ; Male ; Methylation ; Mutation/genetics ; Nuclear Proteins/genetics/metabolism ; Pedigree ; Retinoblastoma-Binding Protein 2/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Structural reorganization of the interleukin-7 signaling complex [Immunology] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-02-15
    Description: We report here an unliganded receptor structure in the common gamma-chain (γc) family of receptors and cytokines. The crystal structure of the unliganded form of the interleukin-7 alpha receptor (IL-7Rα) extracellular domain (ECD) at 2.15 Å resolution reveals a homodimer forming an “X” geometry looking down onto the cell surface with the C termini of the two chains separated by 110 Å and the dimer interface comprising residues critical for IL-7 binding. Further biophysical studies indicate a weak association of the IL-7Rα ECDs but a stronger association between the γc/IL-7Rα ECDs, similar to previous studies of the full-length receptors on CD4+ T cells. Based on these and previous results, we propose a molecular mechanism detailing the progression from the inactive IL-7Rα homodimer and IL-7Rα–γc heterodimer to the active IL-7–IL-7Rα–γc ternary complex whereby the two receptors undergo at least a 90° rotation away from the cell surface, moving the C termini of IL-7Rα and γc from a distance of 110 Å to less than 30 Å at the cell surface. This molecular mechanism can be used to explain recently discovered IL-7– and γc-independent gain-of-function mutations in IL-7Rα from B- and T-cell acute lymphoblastic leukemia patients. The mechanism may also be applicable to other γc receptors that form inactive homodimers and heterodimers independent of their cytokines.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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