Saving, sharing and shaping landrace seeds in commons:unravelling seed commoning norms for furthering agrobiodiversity

One of the major challenges facing agricultural and food systems today is the loss of agrobiodiversity. Considering the current impasse of preventing the worldwide loss of crop diversity, this paper highlights the possibility for a radical reorientation of current legal seed frameworks that could provide more space for alternative seed systems to evolve which centre on norms that support on-farm agrobiodiversity. Understanding the underlying norms that shape seed commons are important, since norms both delimit and contribute to what ultimately will constitute the seeds and who will ultimately have access to the seeds and thus to the extent to which agrobiodiversity is upheld and supported. This paper applies a commoning approach to explore the underpinning norms of a Swedish seed commons initiative and discusses the potential for furthering agrobiodiversity in the context of wider legal and authoritative discourses on seed enclosure. The paper shows how the seed commoning system is shaped and protected by a particular set of farming norms, which allows for sharing seeds among those who adhere to the norms but excludes those who will not. The paper further illustrates how farmers have been able to navigate fragile legal and economic pathways to collectively organize around landrace seeds, which function as an epistemic farming community, that maintain landraces from the past and shape new landraces for the present, adapted to diverse agro-ecological environments for low-input agriculture. The paper reveals how the ascribed norms to the seed commons in combination with the current seed laws set a certain limit to the extent to which agrobiodiversity is upheld and supported and discusses why prescriptions of “getting institutions right” for seed governance are difficult at best, when considering the shifting socio-nature of seeds. To further increase agrobiodiversity, the paper suggests future seed laws are redirected to the sustenance of a proliferation of protected seed commoning systems that can supply locally adapted plant material for diverse groups of farmers and farming systems.</p

Socio-ecological factors determine crop performance in agricultural systems

Agricultural production systems are affected by complex interactions between social and ecological factors, which are often hard to integrate in a common analytical framework. We evaluated differences in crop production among farms by integrating components of several related research disciplines in a single socio-ecological analysis. Specifically, we evaluated spring barley (Hordeum vulgare, L.) performance on 34 farms (organic and conventional) in two agro-ecological zones to unravel the importance of ecological, crop and management factors in the performance of a standard crop. We used Projections to Latent Structures (PLS), a simple but robust analytical tool widely utilized in research disciplines dealing with complex systems (e.g. social sciences and chemometrics), but infrequently in agricultural sciences. We show that barley performance on organic farms was affected by previous management, landscape structure, and soil quality, in contrast to conventional farms where external inputs were the main factors affecting biomass and grain yield. This indicates that more complex management strategies are required in organic than in conventional farming systems. We conclude that the PLS method combining socio-ecological and biophysical factors provides improved understanding of the various interacting factors determining crop performance and can help identify where improvements in the agricultural system are most likely to be effective

Saving, sharing and shaping landrace seeds in commons:unravelling seed commoning norms for furthering agrobiodiversity

One of the major challenges facing agricultural and food systems today is the loss of agrobiodiversity. Considering the current impasse of preventing the worldwide loss of crop diversity, this paper highlights the possibility for a radical reorientation of current legal seed frameworks that could provide more space for alternative seed systems to evolve which centre on norms that support on-farm agrobiodiversity. Understanding the underlying norms that shape seed commons are important, since norms both delimit and contribute to what ultimately will constitute the seeds and who will ultimately have access to the seeds and thus to the extent to which agrobiodiversity is upheld and supported. This paper applies a commoning approach to explore the underpinning norms of a Swedish seed commons initiative and discusses the potential for furthering agrobiodiversity in the context of wider legal and authoritative discourses on seed enclosure. The paper shows how the seed commoning system is shaped and protected by a particular set of farming norms, which allows for sharing seeds among those who adhere to the norms but excludes those who will not. The paper further illustrates how farmers have been able to navigate fragile legal and economic pathways to collectively organize around landrace seeds, which function as an epistemic farming community, that maintain landraces from the past and shape new landraces for the present, adapted to diverse agro-ecological environments for low-input agriculture. The paper reveals how the ascribed norms to the seed commons in combination with the current seed laws set a certain limit to the extent to which agrobiodiversity is upheld and supported and discusses why prescriptions of “getting institutions right” for seed governance are difficult at best, when considering the shifting socio-nature of seeds. To further increase agrobiodiversity, the paper suggests future seed laws are redirected to the sustenance of a proliferation of protected seed commoning systems that can supply locally adapted plant material for diverse groups of farmers and farming systems.</p

Intrinsic plasticity complements long-term potentiation in parallel fiber input gain control in cerebellar Purkinje cells

Synaptic gain control and information storage in neural networks are mediated by alterations in synaptic transmission, such as in long-term potentiation (LTP). Here,weshowusingboth in vitroandin vivo recordingsfromthe rat cerebellum that tetanization protocols for the induction of LTP at parallel fiber (PF)-to-Purkinje cell synapsescanalsoevokeincreases in intrinsic excitability. Thisformof intrinsic plasticity shares with LTP a requirement for the activation of protein phosphatases 1, 2A, and 2B for induction. Purkinje cell intrinsic plasticity resembles CA1 hippocampal pyramidal cell intrinsic plasticity in that it requires activity of protein kinase A(PKA) and casein kinase 2 (CK2) and is mediated by a downregulation of SK-type calcium-sensitive K conductances. In addition, Purkinje cell intrinsic plasticity similarly results in enhanced spine calcium signaling. However, there are fundamental differences: first, while in the hippocampus increases in excitability result in a higher probability for LTP induction, intrinsic plasticity in Purkinj

Genetic variations in A20 DUB domain provide a genetic link to citrullination and neutrophil extracellular traps in systemic lupus erythematosus

Objectives: Genetic variations in TNFAIP3 (A20) de-ubiquitinase (DUB) domain increase the risk of systemic lupus erythematosus (SLE) and rheumatoid arthritis. A20 is a negative regulator of NF-κB but the role of its DUB domain and related genetic variants remain unclear. We aimed to study the functional effects of A20 DUB-domain alterations in immune cells and understand its link to SLE pathogenesis. Methods: CRISPR/Cas9 was used to generate human U937 monocytes with A20 DUB-inactivating C103A knock-in (KI) mutation. Whole genome RNA-sequencing was used to identify differentially expressed genes between WT and C103A KI cells. Functional studies were performed in A20 C103A U937 cells and in immune cells from A20 C103A mice and genotyped healthy individuals with A20 DUB polymorphism rs2230926. Neutrophil extracellular trap (NET) formation was addressed ex vivo in neutrophils from A20 C103A mice and SLE-patients with rs2230926. Results: Genetic disruption of A20 DUB domain in human and murine myeloid cells did not give rise to enhanced NF-κB signalling. Instead, cells with C103A mutation or rs2230926 polymorphism presented an upregulated expression of PADI4, an enzyme regulating protein citrullination and NET formation, two key mechanisms in autoimmune pathology. A20 C103A cells exhibited enhanced protein citrullination and extracellular trap formation, which could be suppressed by selective PAD4 inhibition. Moreover, SLE-patients with rs2230926 showed increased NETs and increased frequency of autoantibodies to citrullinated epitopes. Conclusions: We propose that genetic alterations disrupting the A20 DUB domain mediate increased susceptibility to SLE through the upregulation of PADI4 with resultant protein citrullination and extracellular trap formation

A candidate gene study of the type I interferon pathway implicates IKBKE and IL8 as risk loci for SLE

Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease in which the type I interferon pathway has a crucial role. We have previously shown that three genes in this pathway, IRF5, TYK2 and STAT4, are strongly associated with risk for SLE. Here, we investigated 78 genes involved in the type I interferon pathway to identify additional SLE susceptibility loci. First, we genotyped 896 single-nucleotide polymorphisms in these 78 genes and 14 other candidate genes in 482 Swedish SLE patients and 536 controls. Genes with P<0.01 in the initial screen were then followed up in 344 additional Swedish patients and 1299 controls. SNPs in the IKBKE, TANK, STAT1, IL8 and TRAF6 genes gave nominal signals of association with SLE in this extended Swedish cohort. To replicate these findings we extracted data from a genomewide association study on SLE performed in a US cohort. Combined analysis of the Swedish and US data, comprising a total of 2136 cases and 9694 controls, implicates IKBKE and IL8 as SLE susceptibility loci (Pmeta=0.00010 and Pmeta=0.00040, respectively). STAT1 was also associated with SLE in this cohort (Pmeta=3.3 × 10−5), but this association signal appears to be dependent of that previously reported for the neighbouring STAT4 gene. Our study suggests additional genes from the type I interferon system in SLE, and highlights genes in this pathway for further functional analysis

Complement C4 Copy Number Variation is Linked to SSA/Ro and SSB/La Autoantibodies in Systemic Inflammatory Autoimmune Diseases

Objective Copy number variation of the C4 complement components, C4A and C4B, has been associated with systemic inflammatory autoimmune diseases. This study was undertaken to investigate whether C4 copy number variation is connected to the autoimmune repertoire in systemic lupus erythematosus (SLE), primary Sjögren's syndrome (SS), or myositis. Methods Using targeted DNA sequencing, we determined the copy number and genetic variants of C4 in 2,290 well-characterized Scandinavian patients with SLE, primary SS, or myositis and 1,251 healthy controls. Results A prominent relationship was observed between C4A copy number and the presence of SSA/SSB autoantibodies, which was shared between the 3 diseases. The strongest association was detected in patients with autoantibodies against both SSA and SSB and 0 C4A copies when compared to healthy controls (odds ratio [OR] 18.0 [95% confidence interval (95% CI) 10.2–33.3]), whereas a weaker association was seen in patients without SSA/SSB autoantibodies (OR 3.1 [95% CI 1.7–5.5]). The copy number of C4 correlated positively with C4 plasma levels. Further, a common loss-of-function variant in C4A leading to reduced plasma C4 was more prevalent in SLE patients with a low copy number of C4A. Functionally, we showed that absence of C4A reduced the individuals’ capacity to deposit C4b on immune complexes. Conclusion We show that a low C4A copy number is more strongly associated with the autoantibody repertoire than with the clinically defined disease entities. These findings may have implications for understanding the etiopathogenetic mechanisms of systemic inflammatory autoimmune diseases and for patient stratification when taking the genetic profile into account.publishedVersio

Mapping and assessment of forest ecosystems and their services - Applications and guidance for decision making in the framework of MAES

The aim of this report is to illustrate by means of a series of case studies the implementation of mapping and assessment of forest ecosystem services in different contexts and geographical levels. Methodological aspects, data issues, approaches, limitations, gaps and further steps for improvement are analysed for providing good practices and decision making guidance. The EU initiative on Mapping and Assessment of the state of Ecosystems and their Services (MAES), with the support of all Member States, contributes to improve the knowledge on ecosystem services. MAES is one of the building-block initiatives supporting the EU Biodiversity Strategy to 2020.JRC.H.3-Forest Resources and Climat

Transancestral mapping and genetic load in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease with marked gender and ethnic disparities. We report a large transancestral association study of SLE using Immunochip genotype data from 27,574 individuals of European (EA), African (AA) and Hispanic Amerindian (HA) ancestry. We identify 58 distinct non-HLA regions in EA, 9 in AA and 16 in HA (B50% of these regions have multiple independent associations); these include 24 novel SLE regions (Po5 10 8), refined association signals in established regions, extended associations to additional ancestries, and a disentangled complex HLA multigenic effect. The risk allele count (genetic load) exhibits an accelerating pattern of SLE risk, leading us to posit a cumulative hit hypothesis for autoimmune disease. Comparing results across the three ancestries identifies both ancestry-dependent and ancestry-independent contributions to SLE risk. Our results are consistent with the unique and complex histories of the populations sampled, and collectively help clarify the genetic architecture and ethnic disparities in SL