Enhancement of Late Successional Plants on Ex-Arable Land by Soil Inoculations

Restoration of species-rich grasslands on ex-arable land can help the conservation of biodiversity but faces three big challenges: absence of target plant propagules, high residual soil fertility and restoration of soil communities. Seed additions and top soil removal can solve some of these constraints, but restoring beneficial biotic soil conditions remains a challenge. Here we test the hypotheses that inoculation of soil from late secondary succession grasslands in arable receptor soil enhances performance of late successional plants, especially after top soil removal but pending on the added dose. To test this we grew mixtures of late successional plants in arable top (organic) soil or in underlying mineral soil mixed with donor soil in small or large proportions. Donor soils were collected from different grasslands that had been under restoration for 5 to 41 years, or from semi-natural grassland that has not been used intensively. Donor soil addition, especially when collected from older restoration sites, increased plant community biomass without altering its evenness. In contrast, addition of soil from semi-natural grassland promoted plant community evenness, and hence its diversity, but reduced community biomass. Effects of donor soil additions were stronger in mineral than in organic soil and larger with bigger proportions added. The variation in plant community composition was explained best by the abundances of nematodes, ergosterol concentration and soil pH. We show that in controlled conditions inoculation of soil from secondary succession grassland into ex-arable land can strongly promote target plant species, and that the role of soil biota in promoting target plant species is greatest when added after top soil removal. Together our results point out that transplantation of later secondary succession soil can promote grassland restoration on ex-arable land

Where less may be more: how the rare biosphere pulls ecosystems strings

Rare species are increasingly recognized as crucial, yet vulnerable components of Earth’s ecosystems. This is also true for microbial communities, which are typically composed of a high number of relatively rare species. Recent studies have demonstrated that rare species can have an over-proportional role in biogeochemical cycles and may be a hidden driver of microbiome function. In this review, we provide an ecological overview of the rare microbial biosphere, including causes of rarity and the impacts of rare species on ecosystem functioning. We discuss how rare species can have a preponderant role for local biodiversity and species turnover with rarity potentially bound to phylogenetically conserved features. Rare microbes may therefore be overlooked keystone species regulating the functioning of host-associated, terrestrial and aquatic environments. We conclude this review with recommendations to guide scientists interested in investigating this rapidly emerging research area

Corrigendum:Local and macroscopic electrostatic interactions in single α-helices

The non-covalent forces that stabilise protein structures are not fully understood. One way to address this is to study equilibria between unfolded states and α-helices in peptides. For these, electrostatic forces are believed to contribute, including interactions between: side chains; the backbone and side chains; and side chains and the helix macrodipole. Here we probe these experimentally using designed peptides. We find that both terminal backbone-side chain and certain side chain-side chain interactions (i.e., local effects between proximal charges, or interatomic contacts) contribute much more to helix stability than side chain-helix macrodipole electrostatics, which are believed to operate at larger distances. This has implications for current descriptions of helix stability, understanding protein folding, and the refinement of force fields for biomolecular modelling and simulations. In addition, it sheds light on the stability of rod-like structures formed by single α-helices that are common in natural proteins including non-muscle myosins

The relationship of the musculocutaneous nerve to the brachial plexus evaluated by MRI

Axillary plexus blocks (AXB) are widely used for upper limb operations. It is recommend that AXB should be performed using a multiple injection technique. Information about the course and position of the musculocutaneous nerve (MCN) is of relevance for AXB performance. The objective of this study was to examine the position of the MCN and its relationship to the axillary sheath using MRI. 54 patients underwent an AXB with 40 ml of local anaesthetic before MRI examination. The course of the MCN and the position where it left the axillary sheath and perforated the coracobrachial muscle (MCN exit point), in relation to the axillary artery and the block needle insertion point in the axillary fold, were recorded. The MCN was seen clearly in 23, partly in 26, and not identified in five patients at the MCN exit point. The mean distance from the insertion point of the block needle in the axillary fold to the MCN exit point was 36.8 mm (SD = 18.9, range: 0–90.5). In 37 patients the MCN exit point was positioned inside the Q(1) quadrant (lateral anterior to the axillary artery) and in 11 patients inside the Q(2) quadrant (medial anterior to the axillary artery). There is a wide variability as to where the musculocutaneous nerve (MCN) leaves the axillary sheath. Therefore multiple injection techniques, or the use of a proximally directed catheter, should be appropriate to block the MCN

Mutant ubiquitin found in Alzheimer's disease causes neuritic beading of mitochondria in association with neuronal degeneration

A dinucleotide deletion in human ubiquitin (Ub) B messenger RNA leads to formation of polyubiquitin (UbB) + 1, which has been implicated in neuronal cell death in Alzheimer’s and other neurodegenerative diseases. Previous studies demonstrate that UbB + 1 protein causes proteasome dysfunction. However, the molecular mechanism of UbB + 1-mediated neuronal degeneration remains unknown. We now report that UbB + 1 causes neuritic beading, impairment of mitochondrial movements, mitochondrial stress and neuronal degeneration in primary neurons. Transfection of UbB + 1 induced a buildup of mitochondria in neurites and dysregulation of mitochondrial motor proteins, in particular, through detachment of P74, the dynein intermediate chain, from mitochondria and decreased mitochondria–microtubule interactions. Altered distribution of mitochondria was associated with activation of both the mitochondrial stress and p53 cell death pathways. These results support the hypothesis that neuritic clogging of mitochondria by UbB + 1 triggers a cascade of events characterized by local activation of mitochondrial stress followed by global cell death. Furthermore, UbB + 1 small interfering RNA efficiently blocked expression of UbB + 1 protein, attenuated neuritic beading and preserved cellular morphology, suggesting a potential neuroprotective strategy for certain neurodegenerative disorders