73 research outputs found
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Session A3: Think Big: Adding Large Structures To Improve Ecosystem Health
Abstract:
The Vindel River is one of the few freeflowing its entire catchment are part of the Natura 2000 network. The river was exploited for timber floating between 1850–1976; rapids in the main channel and tributaries below the alpine tree line were channelized to increase timber transport capacity. Side channels were cut off and the flow was concentrated to a single channel from which boulders and large wood were removed. Hence, previously heterogeneous environments were replaced by more homogeneous systems with limited habitat for riverine species. The Vindel River LIFE project (LIFE08 NAT/S/000266) works with the restoration of 25 tributaries in the Vindel River system. The project strives to alleviate the effects of fragmentation and channelization in affected rapids, to improve the quality of water and riparian habitats. The work has included the construction of over 1000 spawning grounds for brown trout, removal of 17 splash dams, the relocation of rocks into the channels, and the strategic placement of large boulders and dead wood in over 50 km of river.
Follow up studies have been done in the channels that have been restored with “demonstration methods,” where previously best-practice restored reaches have been re-restored by adding large boulders and large wood (i.e., entire trees, including root wads) from adjacent upland to the channel. The demonstration restoration has generated wider and more complex streams, which in turn has led to more variable water flow and higher water levels. This will decrease the risk of erosion during high flow and reduce the risk of losing spawning areas. However, fish population data collected by electrofishing before and after restoration show very inconsistent results among tributaries. This highlights the need for considering potential catchment scale degradation and not only concentrating on reach scale problems in order to re-establish ecosystem health
Metabolic control of arginine and ornithine levels paces the progression of leaf senescence
Pools of arginine and ornithine generated during protein degradation can pace the progression of leaf senescence by affecting the TCA cycle, polyamine biosynthesis and the ethylene signaling pathway.Leaf senescence can be induced by stress or aging, sometimes in a synergistic manner. It is generally acknowledged that the ability to withstand senescence-inducing conditions can provide plants with stress resilience. Although the signaling and transcriptional networks responsible for a delayed senescence phenotype, often referred to as a functional stay-green trait, have been actively investigated, very little is known about the subsequent metabolic adjustments conferring this aptitude to survival. First, using the individually darkened leaf (IDL) experimental setup, we compared IDLs of wild-type (WT) Arabidopsis (Arabidopsis thaliana) to several stay-green contexts, that is IDLs of two functional stay-green mutant lines, oresara1-2 (ore1-2) and an allele of phytochrome-interacting factor 5 (pif5), as well as to leaves from a WT plant entirely darkened (DP). We provide compelling evidence that arginine and ornithine, which accumulate in all stay-green contexts-likely due to the lack of induction of amino acids (AAs) transport-can delay the progression of senescence by fueling the Krebs cycle or the production of polyamines (PAs). Secondly, we show that the conversion of putrescine to spermidine (SPD) is controlled in an age-dependent manner. Thirdly, we demonstrate that SPD represses senescence via interference with ethylene signaling by stabilizing the ETHYLENE BINDING FACTOR1 and 2 (EBF1/2) complex. Taken together, our results identify arginine and ornithine as central metabolites influencing the stress- and age-dependent progression of leaf senescence. We propose that the regulatory loop between the pace of the AA export and the progression of leaf senescence provides the plant with a mechanism to fine-tune the induction of cell death in leaves, which, if triggered unnecessarily, can impede nutrient remobilization and thus plant growth and survival
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