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  • 1
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    Ecosystem energetic implications of parasite and free-living biomass in three estuaries (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-25
    Description: Parasites can have strong impacts but are thought to contribute little biomass to ecosystems. We quantified the biomass of free-living and parasitic species in three estuaries on the Pacific coast of California and Baja California. Here we show that parasites have substantial biomass in these ecosystems. We found that parasite biomass exceeded that of top predators. The biomass of trematodes was particularly high, being comparable to that of the abundant birds, fishes, burrowing shrimps and polychaetes. Trophically transmitted parasites and parasitic castrators subsumed more biomass than did other parasitic functional groups. The extended phenotype biomass controlled by parasitic castrators sometimes exceeded that of their uninfected hosts. The annual production of free-swimming trematode transmission stages was greater than the combined biomass of all quantified parasites and was also greater than bird biomass. This biomass and productivity of parasites implies a profound role for infectious processes in these estuaries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuris, Armand M -- Hechinger, Ryan F -- Shaw, Jenny C -- Whitney, Kathleen L -- Aguirre-Macedo, Leopoldina -- Boch, Charlie A -- Dobson, Andrew P -- Dunham, Eleca J -- Fredensborg, Brian L -- Huspeni, Todd C -- Lorda, Julio -- Mababa, Luzviminda -- Mancini, Frank T -- Mora, Adrienne B -- Pickering, Maria -- Talhouk, Nadia L -- Torchin, Mark E -- Lafferty, Kevin D -- England -- Nature. 2008 Jul 24;454(7203):515-8. doi: 10.1038/nature06970.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology, Evolution and Marine Biology and Marine Science Institute, University of California, Santa Barbara, California 93106, USA. kuris@lifesci.ucsb.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18650923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomass ; California ; *Ecosystem ; Host-Parasite Interactions ; Pacific Ocean ; Parasites/*isolation & purification/*physiology ; Snails/parasitology ; Trematoda/isolation & purification/physiology ; Trematode Infections/parasitology ; Wetlands
    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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  • 2
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    Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-10-08
    Description: Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood. Unbiased systems genetics approaches in the rat now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-alpha and PGC1alpha (which are master regulators of mitochondrial and cardiac function), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189541/" 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/PMC3189541/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDermott-Roe, Chris -- Ye, Junmei -- Ahmed, Rizwan -- Sun, Xi-Ming -- Serafin, Anna -- Ware, James -- Bottolo, Leonardo -- Muckett, Phil -- Canas, Xavier -- Zhang, Jisheng -- Rowe, Glenn C -- Buchan, Rachel -- Lu, Han -- Braithwaite, Adam -- Mancini, Massimiliano -- Hauton, David -- Marti, Ramon -- Garcia-Arumi, Elena -- Hubner, Norbert -- Jacob, Howard -- Serikawa, Tadao -- Zidek, Vaclav -- Papousek, Frantisek -- Kolar, Frantisek -- Cardona, Maria -- Ruiz-Meana, Marisol -- Garcia-Dorado, David -- Comella, Joan X -- Felkin, Leanne E -- Barton, Paul J R -- Arany, Zoltan -- Pravenec, Michal -- Petretto, Enrico -- Sanchis, Daniel -- Cook, Stuart A -- 087183/Wellcome Trust/United Kingdom -- MC_U120085815/Medical Research Council/United Kingdom -- MC_U120097112/Medical Research Council/United Kingdom -- British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Oct 5;478(7367):114-8. doi: 10.1038/nature10490.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Body Weight/genetics ; Cardiomegaly/*enzymology/genetics/*pathology/physiopathology ; Cell Respiration ; Chromosomes, Mammalian/genetics ; Crosses, Genetic ; Endodeoxyribonucleases/deficiency/genetics/*metabolism ; Female ; Gene Expression Regulation ; Genes, Mitochondrial/genetics ; Hypertrophy, Left Ventricular/enzymology/genetics/pathology/physiopathology ; Lipid Metabolism ; Male ; Mitochondria/genetics/*metabolism/pathology ; Organ Size/genetics ; Quantitative Trait Loci/genetics ; RNA-Binding Proteins/metabolism ; Rats ; Rats, Inbred Strains ; Reactive Oxygen Species/metabolism ; Receptors, Estrogen/metabolism ; Transcription Factors/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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  • 3
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    Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans (2011)
    Nature Publishing Group (NPG)
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    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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  • 4
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    Retinal dystrophy: development retarded by galactose feeding in spontaneously hypertensive rats (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-01-24
    Description: Retinal photoreceptor cell dystrophies have been widely observed in humans and in animals, but pathogenetic mechanisms are known in only a few such disorders, and successful therapeutic intervention has been reported in fewer still. Spontaneously hypertensive albino rats develop a retinal photoreceptor cell dystrophy with onset late in the first year or early in the second year of life. Between 60 and 70 percent of the animals are affected. A substantial reduction in the prevalence and severity of the dystrophy occurred in such animals whose diet contained 30 percent (by weight) D-galactose. Neither an inhibitor of the enzyme aldose reductase, present in the diet, nor diabetes mellitus, induced by streptozotocin, had any statistically significant influence on the dystrophy. Ambient light and systolic blood pressure levels also did not seem to influence the course of the disorder. The mechanism by which galactose exerts its effect is unknown, but a mutant enzyme with an elevated Michaelis constant (Km) for galactose is plausible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, R N -- Keirn, R J -- Keirn, G V -- Mancini, M A -- Khoury, J K -- EY-02566/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):376-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941900" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Blood Pressure ; Diabetes Mellitus, Experimental/complications ; Female ; Galactose/*therapeutic use ; Humans ; Imidazoles/therapeutic use ; *Imidazolidines ; Rats ; *Rats, Inbred SHR ; *Rats, Inbred Strains ; Retina/pathology ; Retinal Degeneration/complications/*drug therapy/pathology
    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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