Christian Dunn

Peatlands: our greatest source of carbon credits?

Peatlands are the most efficient carbon stores of all terrestrial ecosystems, containing approximately 455 Pg of carbon, which is twice the amount found in the world’s forest biomass. The majority of this carbon is stored in the saturated peat soil. Pristine peatlands are still sequestering carbon at a rate of 0.096 Pg carbon per year; however, anthropogenic degradation of peatlands through draining, fires and exploitation can increase the production of GHGs, switching peatlands from net sinks to net sources of carbon. Conservation of peatlands throughout the UK and the rest of the world is clearly essential for limiting GHG emissions and it is therefore surprising that accounting for emissions from peatlands does not feature prominently in the UNFCCC’s Kyoto Protocol. Discussions at Conference of the Parties (COP) COP-15 and COP-16 look set to make amends for this oversight in any post-2012 climate change legislation, with peatlands becoming important factors in national GHG inventories, the agriculture, forestry and other land use (AFOLU) sector, and in the creation of internationally accredited carbon credits. Using figures from The Economics of Ecosystems and Biodiversity (TEEB), the world’s peatlands can be valued at up to US

Methodologies for Extracellular Enzyme Assays from Wetland Soils

18 billion. However, this sum does not take into account pending UNFCCC decisions. The detailed mandatory inclusion of peatlands in national GHG inventory schemes and in accredited carbon markets could see their value rise even further. This review looks at the current GHG emission-monitoring legislation regarding peatlands, with special focus given to those in the UK. It discusses the importance of peatlands in carbon sequestration, reviews how peatlands feature in current GHG emission-monitoring schemes, concentrating on those associated with the Kyoto Protocol, and considers how peatlands may feature in national GHG emission-monitoring schemes and carbon markets in the future.

Plant Species Effects on the Carbon Storage Capabilities of a Blanket bog Complex

Measurement of extracellular enzymic activity in wetland soils can give an indication of the ecosystems biogeochemical processes, and rates of nutrient and carbon cycling. Analysis of these have allowed researchers to gain an understanding of the ecosystems’ microbial ecology and how it can be affected by environmental factors. Here we give a detailed description of the assays necessary to determine the activity of a suite of key hydrolase enzymes and phenol oxidases. These enzymes control the rates of decomposition and consequently the production of biogenic greenhouse gases. Knowing the processes responsible for the breakdown of organic matter is therefore essential if it becomes necessary to curb these emissions. Our protocols allow for cost effective analysis of a large number of samples and provide sufficient accuracy to determine differences between soil types. When coupled with contemporary microbial techniques these enzyme assays permit entire biochemical pathways to be determined, giving unparalleled knowledge on the processes involved in wetland ecosystems.

The drinking water contaminant dibromoacetonitrile delays G1-S transition and suppresses Chk1 activation at broken replication forks

Plants are known to influence peatland carbon fluxes both i) directly through respiration and ii) by the production of litter and root exudates, which are then broken down by microbes within the peat matrix. In this study we investigated whether three different plant species typical of a UK blanket bog complex - Calluna vulgaris, Juncus effusus and mixed Sphagnum species - influence the carbon sequestering abilities of the peat that they grow in. To quantify this we measured fluxes of soil derived CO2 and CH4, and extractable levels of dissolved organic carbon (DOC) and phenolics, from peat samples taken from areas dominated by one of the three plant communities. It was found that there were significant differences between the carbon fluxes from the different sites, which we attributed to changes brought about by the vegetation on the pH, phenolic concentrations and extracellular enzyme activities found in the peat matrix. Peat taken from Sphagnum-dominated areas emitted less CO2 than the other two sample groups, and had lower overall DOC concentrations and phenol oxidase activities. Conversely, Juncus-peat had the highest CO2 and CH4 fluxes, along with the greatest phenol oxidase activities. Taking all the results into consideration the plants were ranked in order of their ability to reduce the loss of carbon from the peat soil within which they were growing: Sphagnum > Calluna > Juncus. These results suggest that plant community structures could be altered in order to maximise a peatland’s ability to be used as a carbon store should they need to be managed as part of a carbon stewardship scheme or a geoengineering project – if this was to be the sole management interest in an area of peatland.

Quantifying dissolved organic carbon concentrations in upland catchments using phenolic proxy measurements

Chlorination of drinking water protects humans from water-born pathogens, but it also produces low concentrations of dibromoacetonitrile (DBAN), a common disinfectant by-product found in many water supply systems. DBAN is not mutagenic but causes DNA breaks and elevates sister chromatid exchange in mammalian cells. The WHO issued guidelines for DBAN after it was linked with cancer of the liver and stomach in rodents. How this haloacetonitrile promotes malignant cell transformation is unknown. Using fission yeast as a model, we report here that DBAN delays G1-S transition. DBAN does not hinder ongoing DNA replication, but specifically blocks the serine 345 phosphorylation of the DNA damage checkpoint kinase Chk1 by Rad3 (ATR) at broken replication forks. DBAN is particularly damaging for cells with defects in the lagging-strand DNA polymerase delta. This sensitivity can be explained by the dependency of pol delta mutants on Chk1 activation for survival. We conclude that DBAN targets a process or protein that acts at the start of S phase and is required for Chk1 phosphorylation. Taken together, DBAN may precipitate cancer by perturbing S phase and by blocking the Chk1-dependent response to replication fork damage.