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  • 1
    Publication Date: 2009-05-30
    Description: Permafrost soils in boreal and Arctic ecosystems store almost twice as much carbon as is currently present in the atmosphere. Permafrost thaw and the microbial decomposition of previously frozen organic carbon is considered one of the most likely positive climate feedbacks from terrestrial ecosystems to the atmosphere in a warmer world. The rate of carbon release from permafrost soils is highly uncertain, but it is crucial for predicting the strength and timing of this carbon-cycle feedback effect, and thus how important permafrost thaw will be for climate change this century and beyond. Sustained transfers of carbon to the atmosphere that could cause a significant positive feedback to climate change must come from old carbon, which forms the bulk of the permafrost carbon pool that accumulated over thousands of years. Here we measure net ecosystem carbon exchange and the radiocarbon age of ecosystem respiration in a tundra landscape undergoing permafrost thaw to determine the influence of old carbon loss on ecosystem carbon balance. We find that areas that thawed over the past 15 years had 40 per cent more annual losses of old carbon than minimally thawed areas, but had overall net ecosystem carbon uptake as increased plant growth offset these losses. In contrast, areas that thawed decades earlier lost even more old carbon, a 78 per cent increase over minimally thawed areas; this old carbon loss contributed to overall net ecosystem carbon release despite increased plant growth. Our data document significant losses of soil carbon with permafrost thaw that, over decadal timescales, overwhelms increased plant carbon uptake at rates that could make permafrost a large biospheric carbon source in a warmer world.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schuur, Edward A G -- Vogel, Jason G -- Crummer, Kathryn G -- Lee, Hanna -- Sickman, James O -- Osterkamp, T E -- England -- Nature. 2009 May 28;459(7246):556-9. doi: 10.1038/nature08031.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Florida, Gainesville, Florida 32611, USA. tschuur@ufl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478781" target="_blank"〉PubMed〈/a〉
    Keywords: Alaska ; Atmosphere/chemistry ; Carbon/*analysis/metabolism ; Carbon Dioxide/analysis/metabolism ; Carbon Radioisotopes ; *Cold Climate ; *Ecosystem ; Feedback ; *Freezing ; *Greenhouse Effect ; Phase Transition ; Soil/*analysis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2012-10-24
    Description: Arginine methylation of histones is a well-known regulator of gene expression. Protein arginine methyltransferase 6 (PRMT6) has been shown to function as a transcriptional repressor by methylating the histone H3 arginine 2 [H3R2(me2a)] repressive mark; however, few targets are known. To define the physiological role of PRMT6 and to identify its targets, we generated PRMT6 –/– mouse embryo fibroblasts (MEFs). We observed that early passage PRMT6 –/– MEFs had growth defects and exhibited the hallmarks of cellular senescence. PRMT6 –/– MEFs displayed high transcriptional levels of p53 and its targets, p21 and PML. Generation of PRMT6 –/– ; p53 –/– MEFs prevented the premature senescence, suggesting that the induction of senescence is p53-dependent. Using chromatin immunoprecipitation assays, we observed an enrichment of PRMT6 and H3R2(me2a) within the upstream region of Trp53 . The PRMT6 association and the H3R2(me2a) mark were lost in PRMT6 –/– MEFs and an increase in the H3K4(me3) activator mark was observed. Our findings define a new regulator of p53 transcriptional regulation and define a role for PRMT6 and arginine methylation in cellular senescence.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
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