Wetland maps including open water extent dynamics based on ENVISAT ASAR WS for Siberia, 2007 and 2008, links to GeoTIFFs

Wetlands store large amounts of carbon, and depending on their status and type, they release specific amounts of methane gas to the atmosphere. The connection between wetland type and methane emission has been investigated in various studies and utilized in climate change monitoring and modelling. For improved estimation of methane emissions, land surface models require information such as the wetland fraction and its dynamics over large areas. Existing datasets of wetland dynamics present the total amount of wetland (fraction) for each model grid cell, but do not discriminate the different wetland types like permanent lakes, periodically inundated areas or peatlands. Wetland types differently influence methane fluxes and thus their contribution to the total wetland fraction should be quantified. Especially wetlands of permafrost regions are expected to have a strong impact on future climate due to soil thawing. In this study ENIVSAT ASAR Wide Swath data was tested for operational monitoring of the distribution of areas with a long-term SW near 1 (hSW) in northern Russia (SW = degree of saturation with water, 1 = saturated), which is a specific characteristic of peatlands. For the whole northern Russia, areas with hSW were delineated and discriminated from dynamic and open water bodies for the years 2007 and 2008. The area identified with this method amounts to approximately 300,000 km**2 in northern Siberia in 2007. It overlaps with zones of high carbon storage. Comparison with a range of related datasets (static and dynamic) showed that hSW represents not only peatlands but also temporary wetlands associated with post-forest fire conditions in permafrost regions. Annual long-term monitoring of change in boreal and tundra environments is possible with the presented approach. Sentinel-1, the successor of ENVISAT ASAR, will provide data that may allow continuous monitoring of these wetland dynamics in the future complementing global observations of wetland fraction.

Extent of genomic rearrangement after genome duplication in yeast

Whole-genome duplication approximately 108 years ago was proposed as an explanation for the many duplicated chromosomal regions in Saccharomyces cerevisiae. Here we have used computer simulations and analytic methods to estimate some parameters describing the evolution of the yeast genome after this duplication event. Computer simulation of a model in which 8% of the original genes were retained in duplicate after genome duplication, and 70–100 reciprocal translocations occurred between chromosomes, produced arrangements of duplicated chromosomal regions very similar to the map of real duplications in yeast. An analytical method produced an independent estimate of 84 map disruptions. These results imply that many smaller duplicated chromosomal regions exist in the yeast genome in addition to the 55 originally reported. We also examined the possibility of determining the original order of chromosomal blocks in the ancestral unduplicated genome, but this cannot be done without information from one or more additional species. If the genome sequence of one other species (such as Kluyveromyces lactis) were known it should be possible to identify 150–200 paired regions covering the whole yeast genome and to reconstruct approximately two-thirds of the original order of blocks of genes in yeast. Rates of interchromosome translocation in yeast and mammals appear similar despite their very different rates of homologous recombination per kilobase.

The onset and extent of genomic instability in sporadic colorectal tumor progression

Cancer cell genomes contain alterations beyond known etiologic events, but their total number has been unknown at even the order of magnitude level. By sampling colorectal premalignant polyp and carcinoma cell genomes through use of the technique inter-(simple sequence repeat) PCR, we have found genomic alterations to be considerably more abundant than expected, with the mean number of genomic events per carcinoma cell totaling approximately 11,000. Colonic polyps early in the tumor progression pathway showed similar numbers of events. These results indicate that, as with certain hereditary cancer syndromes, genomic destabilization is an early step in sporadic tumor development. Together these results support the model of genomic instability being a cause rather than an effect of malignancy, facilitating vastly accelerated somatic cell evolution, with the observed orderly steps of the colon cancer progression pathway reflecting the consequences of natural selection.