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  • 1
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    Prohibitin couples diapause signalling to mitochondrial metabolism during ageing in C. elegans (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-10-09
    Description: Marked alterations in cellular energy metabolism are a universal hallmark of the ageing process. The biogenesis and function of mitochondria, the energy-generating organelles in eukaryotic cells, are primary longevity determinants. Genetic or pharmacological manipulations of mitochondrial activity profoundly affect the lifespan of diverse organisms. However, the molecular mechanisms regulating mitochondrial biogenesis and energy metabolism during ageing are poorly understood. Prohibitins are ubiquitous, evolutionarily conserved proteins, which form a ring-like, high-molecular-mass complex at the inner membrane of mitochondria. Here, we show that the mitochondrial prohibitin complex promotes longevity by modulating mitochondrial function and fat metabolism in the nematode Caenorhabditis elegans. We found that prohibitin deficiency shortens the lifespan of otherwise wild-type animals. Notably, knockdown of prohibitin promotes longevity in diapause mutants or under conditions of dietary restriction. In addition, prohibitin deficiency extends the lifespan of animals with compromised mitochondrial function or fat metabolism. Depletion of prohibitin influences ATP levels, animal fat content and mitochondrial proliferation in a genetic-background- and age-specific manner. Together, these findings reveal a novel mechanism regulating mitochondrial biogenesis and function, with opposing effects on energy metabolism, fat utilization and ageing in C. elegans. Prohibitin may have a similar key role in modulating energy metabolism during ageing in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Artal-Sanz, Marta -- Tavernarakis, Nektarios -- England -- Nature. 2009 Oct 8;461(7265):793-7. doi: 10.1038/nature08466.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology, Heraklion 71110, Crete, Greece. martal@ibv.csic.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19812672" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Aging/*physiology ; Animals ; Caenorhabditis elegans/genetics/*growth & development/*metabolism/physiology ; Caloric Restriction ; Energy Metabolism/genetics/physiology ; Gene Knockdown Techniques ; Intestines/metabolism ; Lipid Metabolism/genetics/physiology ; Longevity/genetics/physiology ; Mitochondria/*metabolism/physiology ; Mutation/genetics ; Repressor Proteins/genetics/*metabolism ; *Signal Transduction
    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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    Coordination of mitophagy and mitochondrial biogenesis during ageing in C. elegans (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-04-22
    Description: Impaired mitochondrial maintenance in disparate cell types is a shared hallmark of many human pathologies and ageing. How mitochondrial biogenesis coordinates with the removal of damaged or superfluous mitochondria to maintain cellular homeostasis is not well understood. Here we show that mitophagy, a selective type of autophagy targeting mitochondria for degradation, interfaces with mitochondrial biogenesis to regulate mitochondrial content and longevity in Caenorhabditis elegans. We find that DCT-1 is a key mediator of mitophagy and longevity assurance under conditions of stress in C. elegans. Impairment of mitophagy compromises stress resistance and triggers mitochondrial retrograde signalling through the SKN-1 transcription factor that regulates both mitochondrial biogenesis genes and mitophagy by enhancing DCT-1 expression. Our findings reveal a homeostatic feedback loop that integrates metabolic signals to coordinate the biogenesis and turnover of mitochondria. Uncoupling of these two processes during ageing contributes to overproliferation of damaged mitochondria and decline of cellular function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palikaras, Konstantinos -- Lionaki, Eirini -- Tavernarakis, Nektarios -- England -- Nature. 2015 May 28;521(7553):525-8. doi: 10.1038/nature14300. Epub 2015 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece [2] Department of Biology, University of Crete, Heraklion 70013, Crete, Greece. ; Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece. ; 1] Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece [2] Department of Basic Sciences, Faculty of Medicine, University of Crete, Heraklion 71110, Crete, Greece.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25896323" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/pathology/*physiology ; Animals ; Caenorhabditis elegans/*cytology/genetics/*physiology ; Caenorhabditis elegans Proteins/metabolism ; DNA-Binding Proteins/metabolism ; Homeostasis ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Longevity ; Membrane Proteins/metabolism ; Mitochondria/genetics/*metabolism/pathology ; *Mitochondrial Degradation/genetics ; Signal Transduction ; Stress, Physiological ; 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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    Small heat-shock proteins protect from heat-stroke-associated neurodegeneration (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-09-14
    Description: Heat stroke is a life-threatening condition, characterized by catastrophic collapse of thermoregulation and extreme hyperthermia. In recent years, intensification of heat waves has caused a surge of heat-stroke fatalities. The mechanisms underlying heat-related pathology are poorly understood. Here we show that heat stroke triggers pervasive necrotic cell death and neurodegeneration in Caenorhabditis elegans. Preconditioning of animals at a mildly elevated temperature strongly protects from heat-induced necrosis. The heat-shock transcription factor HSF-1 and the small heat-shock protein HSP-16.1 mediate cytoprotection by preconditioning. HSP-16.1 localizes to the Golgi, where it functions with the Ca(2+)- and Mn(2+)-transporting ATPase PMR-1 to maintain Ca(2+) homeostasis under heat stroke. Preconditioning also suppresses cell death inflicted by diverse insults, and protects mammalian neurons from heat cytotoxicity. These findings reveal an evolutionarily conserved mechanism that defends against diverse necrotic stimuli, and may be relevant to heat stroke and other pathological conditions involving necrosis in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kourtis, Nikos -- Nikoletopoulou, Vassiliki -- Tavernarakis, Nektarios -- England -- Nature. 2012 Oct 11;490(7419):213-8. doi: 10.1038/nature11417. Epub 2012 Sep 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology, Heraklion 71110, Crete, Greece.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22972192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/*metabolism ; Caenorhabditis elegans Proteins/genetics/metabolism ; Calcium/metabolism ; Calcium-Transporting ATPases/genetics/metabolism ; Cells, Cultured ; Cytoplasm/metabolism ; Heat-Shock Proteins, Small/*metabolism ; Heat-Shock Response/*physiology ; Hot Temperature ; Larva ; Mice ; Mutation ; Necrosis/etiology/physiopathology ; Neurons/*pathology ; Survival Analysis
    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
    Electronic Resource
    Electronic Resource
    Genetic evidence for functional specificity of the yeast GCN2 kinase (1996)
    Springer
    Molecular genetics and genomics 251 (1996), S. 613-618 
    Details
    ISSN: 1617-4623
    Keywords: GCN4 ; eIF-2 ; DAI kinase ; tRNA ; Translational regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In yeast the GCN2 kinase mediates translational control ofGCN4 by phosphorylating the α subunit of eIF-2 in response to extracellular amino acid limitation. Although phosphorylation of eIF-2α has been shown to inhibit global protein synthesis, amino acid starvation results in a specific activation effect onGCN4 mRNA translation. Under the same conditions, translation of other mRNAs appears only slightly affected. The mechanism responsible for the observed selectivity of the GCN2 kinase is not clear. Here, we present genetic evidence that suggests that locally restricted action of the GCN2 kinase facilitatesGCN4-specific translational regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02173652
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  • 5
    Electronic Resource
    Electronic Resource
    The DNA target sequence influences the dependence of the yeast transcriptional activator Gcn4 on co-factors (1997)
    Springer
    Molecular genetics and genomics 253 (1997), S. 766-769 
    Details
    ISSN: 1617-4623
    Keywords: Key words Ada2 ; Gcn5 ; Ap1 site ; Upstream Activating Sequences ; Transcriptional regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  The yeast transcriptional activator Gcn4 requires the Ada2/Gcn5/Ada3 co-activator complex to exert part of its activation potential. Here we show that the sequence of the DNA target modulates the function of Gcn4 by modifying this requirement. Promoter configurations were generated that rendered Gcn4-induced transcription either completely dependent or completely independent of the Ada2/ Gcn5/Ada3 complex. The topological constraints imposed by these configurations suggest that Gcn4 makes multiple contacts with the basic transcription machinery that are subject to modification by the incident DNA target. We propose that these modifications further determine the direction on the chromosome in which an otherwise symmetric, dimeric transcription factor will activate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004380050382
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  • 6
    Electronic Resource
    Electronic Resource
    Acquisition of a potential marker for insect transformation: isolation of a novel alcohol dehydrogenase gene from Bactrocera oleae by functional complementation in yeast (2000)
    Springer
    Molecular genetics and genomics 263 (2000), S. 90-95 
    Details
    ISSN: 1617-4623
    Keywords: Key wordsDrosophila melanogaster ; Ceratitis capitata ; Tephritids ; Evolution ; Dacus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The alcohol dehydrogenase genes make up one of the best studied gene families in Drosophila, both in terms of expression and evolution. Moreover, alcohol dehydrogenase genes constitute potential versatile markers in insect transformation experiments. However, due to their rapid evolution, these genes cannot be cloned from other insect genera by DNA hybridization or PCR-based strategies. We have therefore explored an alternative strategy: cloning by functional complementation of appropriate yeast mutants. Here we report that two alcohol dehydrogenase genes from the medfly Ceratitis capitata can functionally replace the yeast enzymes, even though the medfly and yeast genes have evolved independently, acquiring their enzymatic function convergently. Using this method, we have cloned an alcohol dehydrogenase gene from the olive pest Bactrocera oleae. We conclude that functional complementation in yeast can be used to clone alcohol dehydrogenase genes that are unrelated in sequence to those of yeast, thus providing a powerful tool for isolation of dominant insect transformation marker genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00008679
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  • 7
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    Genetically targeted cell disruption in Caenorhabditis elegans (1997)
    National Academy of Sciences
    Details
    Publication Date: 1997-11-25
    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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  • 8
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    Caloric restriction and resveratrol promote longevity through the Sirtuin-1-dependent induction of autophagy (2010)
    Springer Nature
    Details
    Publication Date: 2010-01-01
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 9
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    Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 (2014)
    Springer Nature
    Details
    Publication Date: 2014-09-19
    Print ISSN: 1350-9047
    Electronic ISSN: 1476-5403
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 10
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    No death without life: vital functions of apoptotic effectors (2008)
    Springer Nature
    Details
    Publication Date: 2008-02-29
    Print ISSN: 1350-9047
    Electronic ISSN: 1476-5403
    Topics: Biology , Medicine
    Published by Springer Nature
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