Stock of standing dead trees in boreal forests of Central Siberia

A significant part of carbon assimilated by forest is deposited in tree trunks. Growth and development of tree stands is accompanied by accumulation of standing dead trees (snags) due to natural tree mortality and as a result of the impact of exogenous factors. Carbon accumulated in these dead trunks is excluded from the fast turnover due to low rate of wood decomposition, so that snags can be considered as a pool of organic carbon with a slow rate of its return to the atmosphere. We estimated stock of snags on 54 sample plots, which represent the main types of forest ecosystems in the northern and middle taiga of Central Siberia. In the middle taiga, stock of snags varied from up to 7 m3 ha-1 in Siberian spruce forests to 20-42 m3 ha-1 in Scots pine forests. Larch forests in the northern taiga had the similar stock of snags as larch forests in the middle taiga despite significantly higher growing stock in the later. Snags contributed from 4 to 19% to the total stock of woody biomass in studied forests. This study indicated the significance of snags and can be used to estimate carbon budget of forest ecosystems of the region

A mitochondria-specific mutational signature of aging: increased rate of A > G substitutions on the heavy strand.

The mutational spectrum of the mitochondrial DNA (mtDNA) does not resemble any of the known mutational signatures of the nuclear genome and variation in mtDNA mutational spectra between different organisms is still incomprehensible. Since mitochondria are responsible for aerobic respiration, it is expected that mtDNA mutational spectrum is affected by oxidative damage. Assuming that oxidative damage increases with age, we analyse mtDNA mutagenesis of different species in regards to their generation length. Analysing, (i) dozens of thousands of somatic mtDNA mutations in samples of different ages (ii) 70053 polymorphic synonymous mtDNA substitutions reconstructed in 424 mammalian species with different generation lengths and (iii) synonymous nucleotide content of 650 complete mitochondrial genomes of mammalian species we observed that the frequency of AH > GH substitutions (H: heavy strand notation) is twice bigger in species with high versus low generation length making their mtDNA more AH poor and GH rich. Considering that AH > GH substitutions are also sensitive to the time spent single-stranded (TSSS) during asynchronous mtDNA replication we demonstrated that AH > GH substitution rate is a function of both species-specific generation length and position-specific TSSS. We propose that AH > GH is a mitochondria-specific signature of oxidative damage associated with both aging and TSSS