191 research outputs found

    Photosynthetic limits on carbon sequestration in croplands

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    This is the final version. Available on open access from Elsevier via the DOI in this recordHow much C can be stored in agricultural soils worldwide to mitigate rising carbon dioxide (CO2) concentrations, and at what cost? This question, because of its critical relevance to climate policy, has been a focus of soil science for decades. The amount of additional soil organic C (SOC) that could be stored has been estimated in various ways, most of which have taken the soil as the starting point: projecting how much of the SOC previously lost can be restored, for example, or calculating the cumulative effect of multiple soil management strategies. Here, we take a different approach, recognizing that photosynthesis, the source of C input to soil, represents the most fundamental constraint to C sequestration. We follow a simple “Fermi approach” to derive a rough but robust estimate by reducing our problem to a series of approximate relations that can be parameterized using data from the literature. We distinguish two forms of soil C: ‘ephemeral C’, denoting recently-applied plant-derived C that is quickly decayed to CO2, and ‘lingering C,’ which remains in the soil long enough to serve as a lasting repository for C derived from atmospheric CO2. First, we estimate global net C inputs into lingering SOC in croplands from net primary production, biomass removal by humans and short-term decomposition. Next, we estimate net additional C storage in cropland soils globally from the estimated C inputs, accounting also for decomposition of lingering SOC already present. Our results suggest a maximum C input rate into the lingering SOC pool of 0.44 Pg C yr−1, and a maximum net sequestration rate of 0.14 Pg C yr−1 – significantly less than most previous estimates, even allowing for acknowledged uncertainties. More importantly, we argue for a re-orientation in emphasis from soil processes towards a wider ecosystem perspective, starting with photosynthesis.Biotechnology and Biological Sciences Research Council (BBSRC

    Nitrogen and sulphur management: challenges for organic sources in temperate agricultural systems

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    A current global trend towards intensification or specialization of agricultural enterprises has been accompanied by increasing public awareness of associated environmental consequences. Air and water pollution from losses of nutrients, such as nitrogen (N) and sulphur (S), are a major concern. Governments have initiated extensive regulatory frameworks, including various land use policies, in an attempt to control or reduce the losses. This paper presents an overview of critical input and loss processes affecting N and S for temperate climates, and provides some background to the discussion in subsequent papers evaluating specific farming systems. Management effects on potential gaseous and leaching losses, the lack of synchrony between supply of nutrients and plant demand, and options for optimizing the efficiency of N and S use are reviewed. Integration of inorganic and organic fertilizer inputs and the equitable re-distribution of nutrients from manure are discussed. The paper concludes by highlighting a need for innovative research that is also targeted to practical approaches for reducing N and S losses, and improving the overall synchrony between supply and demand

    Turnover of Carbohydrate-Rich Vegetal Matter During Microaerobic Composting and After Amendment in Soil

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    We propose that microaerobic composting (MC) can be used to decompose vegetal matter with a short turnover time and large carbon (C) recycling potential. We used a novel method for measuring the degree of fragmentation of water-insoluble acid-soluble (WIAS) polysaccharides as a proxy in tracking their relative degree of degradation (i.e., fragmentation endpoint index). Oak leaves and food scrap processed by MC reached a fragmentation end point within 2 weeks. After amending the MC products into soil, the half-life of the polysaccharide residues was ~6–7 times longer (~100–110 days) than that measured during MC. The main products given up during MC were volatile organic acids (VOAs), alcohols and soluble carbohydrates in the compost tea, and CO2. These products accounted for about 2% of the initial carbon in the feedstock. Very small amounts of VOAs, particularly butyric acid, were formed in the amended soil. Based on a residence time of materials in fermentors of 2 weeks, a ~100-m3 capacity MC facility could process 2,000–4,000 metric tons of vegetable matter amended in ten hectares of arable land per year

    The Histone H3K79 Methyltransferase Dot1L Is Essential for Mammalian Development and Heterochromatin Structure

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    Dot1 is an evolutionarily conserved histone methyltransferase specific for lysine 79 of histone H3 (H3K79). In Saccharomyces cerevisiae, Dot1-mediated H3K79 methylation is associated with telomere silencing, meiotic checkpoint control, and DNA damage response. The biological function of H3K79 methylation in mammals, however, remains poorly understood. Using gene targeting, we generated mice deficient for Dot1L, the murine Dot1 homologue. Dot1L-deficient embryos show multiple developmental abnormalities, including growth impairment, angiogenesis defects in the yolk sac, and cardiac dilation, and die between 9.5 and 10.5 days post coitum. To gain insights into the cellular function of Dot1L, we derived embryonic stem (ES) cells from Dot1L mutant blastocysts. Dot1L-deficient ES cells show global loss of H3K79 methylation as well as reduced levels of heterochromatic marks (H3K9 di-methylation and H4K20 tri-methylation) at centromeres and telomeres. These changes are accompanied by aneuploidy, telomere elongation, and proliferation defects. Taken together, these results indicate that Dot1L and H3K79 methylation play important roles in heterochromatin formation and in embryonic development

    The conservation and uniqueness of the caspase family in the basal chordate, amphioxus

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    <p>Abstract</p> <p>Background</p> <p>The caspase family, which plays a central role in apoptosis in metazoans, has undergone an expansion in amphioxus, increasing to 45 members through domain recombination and shuffling.</p> <p>Results</p> <p>In order to shed light on the conservation and uniqueness of this family in amphioxus, we cloned three representative caspase genes, designated as <it>bbtCaspase-8, bbtCaspase-1/2 </it>and <it>bbtCaspase3</it>-like, from the amphioxus <it>Branchiostoma belcheri tsingtauense</it>. We found that <it>bbtCaspase-8 </it>with conserved protein architecture is involved in the Fas-associated death domain-Caspase-8 mediated pro-apoptotic extrinsic pathway, while <it>bbtCaspase3</it>-like may mediate a nuclear apoptotic pathway in amphioxus. Also, <it>bbtCaspase-1/2 </it>can co-localize with <it>bbtFADD2 </it>in the nucleus, and be recruited to the cytoplasm by amphioxus apoptosis associated speck-like proteins containing a caspase recruitment domain, indicating that <it>bbtCaspase-1/2 </it>may serve as a switch between apoptosis and caspase-dependent innate immune response in invertebrates. Finally, amphioxus extrinsic apoptotic pathway related caspases played important roles in early embryogenesis.</p> <p>Conclusions</p> <p>Our study not only demonstrates the conservation of <it>bbtCaspase-8 </it>in apoptosis, but also reveals the unique features of several amphioxus caspases with novel domain architectures arose some 500 million years ago.</p

    Regulation of the DNA Damage Response and Gene Expression by the Dot1L Histone Methyltransferase and the 53Bp1 Tumour Suppressor

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    Dot1L, a histone methyltransferase that targets histone H3 lysine 79 (H3K79), has been implicated in gene regulation and the DNA damage response although its functions in these processes remain poorly defined.Using the chicken DT40 model system, we generated cells in which the Dot1L gene is disrupted to examine the function and focal recruitment of the 53Bp1 DNA damage response protein. Detailed kinetic and dose response assays demonstrate that, despite the absence of H3K79 methylation demonstrated by mass spectrometry, 53Bp1 focal recruitment is not compromised in these cells. We also describe, for the first time, the phenotypes of a cell line lacking both Dot1L and 53Bp1. Dot1L⁻/⁻ and wild type cells are equally resistant to ionising radiation, whereas 53Bp1⁻/⁻/Dot1L⁻/⁻ cells display a striking DNA damage resistance phenotype. Dot1L and 53Bp1 also affect the expression of many genes. Loss of Dot1L activity dramatically alters the mRNA levels of over 1200 genes involved in diverse biological functions. These results, combined with the previously reported list of differentially expressed genes in mouse ES cells knocked down for Dot1L, demonstrates surprising cell type and species conservation of Dot1L-dependent gene expression. In 53Bp1⁻/⁻ cells, over 300 genes, many with functions in immune responses and apoptosis, were differentially expressed. To date, this is the first global analysis of gene expression in a 53Bp1-deficient cell line.Taken together, our results uncover a negative role for Dot1L and H3K79 methylation in the DNA damage response in the absence of 53Bp1. They also enlighten the roles of Dot1L and 53Bp1 in gene expression and the control of DNA double-strand repair pathways in the context of chromatin

    Mst1/2 signalling to Yap: gatekeeper for liver size and tumour development

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    The mechanisms controlling mammalian organ size have long been a source of fascination for biologists. These controls are needed to both ensure the integrity of the body plan and to restrict inappropriate proliferation that could lead to cancer. Regulation of liver size is of particular interest inasmuch as this organ maintains the capacity for regeneration throughout life, and is able to regain precisely its original mass after partial surgical resection. Recent studies using genetically engineered mouse strains have shed new light on this problem; the Hippo signalling pathway, first elucidated as a regulator of organ size in Drosophila, has been identified as dominant determinant of liver growth. Defects in this pathway in mouse liver lead to sustained liver overgrowth and the eventual development of both major types of liver cancer, hepatocellular carcinoma and cholangiocarcinoma. In this review, we discuss the role of Hippo signalling in liver biology and the contribution of this pathway to liver cancer in humans
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