A network approach for managing ecosystem services and improving food and nutrition security on smallholder farms

Smallholder farmers are some of the poorest and most food insecure people on Earth. Their high nutritional and economic reliance on home-grown produce makes them particularly vulnerable to environmental stressors such as pollinator loss or climate change which threaten agricultural productivity. Improving smallholder agriculture in a way that is environmentally sustainable and resilient to climate change is a key challenge of the 21st century. Ecological intensification, whereby ecosystem services are managed to increase agricultural productivity, is a promising solution for smallholders. However, smallholder farms are complex socio-ecological systems with a range of social, ecological and environmental factors interacting to influence ecosystem service provisioning. To truly understand the functioning of a smallholder farm and identify the most effective management options to support household food and nutrition security, a holistic, systems-based understanding is required. In this paper, we propose a network approach to understand, visualise and model the complex interactions occurring among wild species, crops and people on smallholder farms. Specifically, we demonstrate how networks may be used to (a) identify wild species with a key role in supporting, delivering or increasing the resilience of an ecosystem service; (b) quantify the value of an ecosystem service in a way that is relevant to the food and nutrition security of smallholders; and (c) understand the social interactions that influence the management of shared ecosystem services. Using a case study based on data from rural Nepal, we demonstrate how this framework can be used to connect wild plants, pollinators and crops to key nutrients consumed by humans. This allows us to quantify the nutritional value of an ecosystem service and identify the wild plants and pollinators involved in its provision, as well as providing a framework to predict the effects of environmental change on human nutrition. Our framework identifies mechanistic links between ecosystem services and the nutrients consumed by smallholder farmers and highlights social factors that may influence the management of these services. Applying this framework to smallholder farms in a range of socio-ecological contexts may provide new, sustainable and equitable solutions to smallholder food and nutrition security. A free Plain Language Summary can be found within the Supporting Information of this article

Does urbanization explain differences in interactions between an insect herbivore and its natural enemies and mutualists?

Urbanization can alter the composition of arthropod communities. However, little is known about how urbanization affects ecological interactions. Using experimental colonies of the black bean aphid Aphis fabae Scopoli reared on Vicia faba L, we asked if patterns of predator-prey, host-parasitoid and ant-aphid mutualisms varied along an urbanization gradient across a large town in southern England. We recorded the presence of naturally occurring predators, parasitoid wasps and mutualistic ants together with aphid abundance. We examined how biotic (green areas and plant richness) and abiotic features (impervious surfaces and distance to town center) affected (1) aphid colony size, (2) the likelihood of finding predators, mutualistic ants and aphid mummies (indicating the presence of parasitoids), and (3) how the interplay among these factors affected patterns of parasitoid attack, predator abundance, mutualistic interactions and aphid abundance. The best model to predict aphid abundance was the number of mutualistic ants attending the colonies. Aphid predators responded negatively to both the proportion of impervious surfaces and to the number of mutualistic ants farming the colonies, and positively to aphid population size, whereas parasitized aphids were found in colonies with higher numbers of aphids and ants. The number of mutualistic ants attending was positively associated with aphid colony size and negatively with the number of aphid predators. Our findings suggest that for insect-natural enemy interactions, urbanization may affect some groups, while not influencing others, and that local effects (mutualists, host plant presence) will also be key determinants of how urban ecological communities are formed

Reduced body sizes in climate-impacted tropical insect assemblages are primarily explained by range shifts

Both community composition changes due to species redistribution and within-species size shifts may alter body size structures under climate warming. Here we assess the relative contribution of these processes in community-level body size changes in tropical moth assemblages that moved uphill during a period of warming. Based on resurvey data for seven assemblages (>8000 individuals) on Mt. Kinabalu, Borneo in 1965 and 2007, we show significant wing-length reduction (mean shrinkage of 1.3% per species). Range shifts explain most size re-structuring, due to uphill shifts of relatively small species, especially at high elevations. Overall, mean forewing length shrank by ca. 5%, much of which accounted for by species range boundary shifts (3.9%), followed by within-boundary distribution changes (0.5%), and within-species size shrinkage (0.6%). We conclude that the effects of range shifting predominate, but considering species physiological responses is also important for understanding community size reorganization under climate warming

The spatial scaling of species interaction networks

International audienceSpecies-area relationships (SARs) are pivotal to understand the distribution of biodiversity across spatial scales. We know little, however, about how the network of biotic interactions in which biodiversity is embedded changes with spatial extent. Here we develop a new theoretical framework that enables us to explore how different assembly mechanisms and theoretical models affect multiple properties of ecological networks across space. We present a number of testable predictions on network-area relationships (NARs) for multi-trophic communities. Network structure changes as area increases because of the existence of different SARs across trophic levels, the preferential selection of generalist species at small spatial extents and the effect of dispersal limitation promoting beta-diversity. Developing an understanding of NARs will complement the growing body of knowledge on SARs with potential applications in conservation ecology. Specifically, combined with further empirical evidence, NARs can generate predictions of potential effects on ecological communities of habitat loss and fragmentation in a changing world

Specific Variants in the MLH1 Gene Region May Drive DNA Methylation, Loss of Protein Expression, and MSI-H Colorectal Cancer

Background: We previously identified an association between a mismatch repair gene, MLH1, promoter SNP (rs1800734) and microsatellite unstable (MSI-H) colorectal cancers (CRCs) in two samples. The current study expanded on this finding as we explored the genetic basis of DNA methylation in this region of chromosome 3. We hypothesized that specific polymorphisms in the MLH1 gene region predispose it to DNA methylation, resulting in the loss of MLH1 gene expression, mismatch-repair function, and consequently to genome-wide microsatellite instability. Methodology/Principal Findings: We first tested our hypothesis in one sample from Ontario (901 cases, 1,097 controls) and replicated major findings in two additional samples from Newfoundland and Labrador (479 cases, 336 controls) and from Seattle (591 cases, 629 controls). Logistic regression was used to test for association between SNPs in the region of MLH1 and CRC, MSI-H CRC, MLH1 gene expression in CRC, and DNA methylation in CRC. The association between rs1800734 and MSI-H CRCs, previously reported in Ontario and Newfoundland, was replicated in the Seattle sample. Two additional SNPs, in strong linkage disequilibrium with rs1800734, showed strong associations with MLH1 promoter methylation, loss of MLH1 protein, and MSI-H CRC in all three samples. The logistic regression model of MSI-H CRC that included MLH1-promotermethylation status and MLH1 immunohisotchemistry status fit most parsimoniously in all three samples combined. When rs1800734 was added to this model, its effect was not statistically significant (P-value = 0.72 vs. 2.361024 when the SNP was examined alone). Conclusions/Significance: The observed association of rs1800734 with MSI-H CRC occurs through its effect on the MLH1 promoter methylation, MLH1 IHC deficiency, or both

X-Linked Glomerulopathy Due to COL4A5 Founder Variant

Alport syndrome is a rare hereditary disorder caused by rare variants in 1 of 3 genes encoding for type IV collagen. Rare variants in COL4A5 on chromosome Xq22 cause X-linked Alport syndrome, which accounts for ∼80% of the cases. Alport syndrome has a variable clinical presentation, including progressive kidney failure, hearing loss, and ocular defects. Exome sequencing performed in 2 affected related males with an undefined X-linked glomerulopathy characterized by global and segmental glomerulosclerosis, mesangial hypercellularity, and vague basement membrane immune complex deposition revealed a COL4A5 sequence variant, a substitution of a thymine by a guanine at nucleotide 665 (c.T665G; rs281874761) of the coding DNA predicted to lead to a cysteine to phenylalanine substitution at amino acid 222, which was not seen in databases cataloguing natural human genetic variation, including dbSNP138, 1000 Genomes Project release version 01-11-2004, Exome Sequencing Project 21-06-2014, or ExAC 01-11-2014. Review of the literature identified 2 additional families with the same COL4A5 variant leading to similar atypical histopathologic features, suggesting a unique pathologic mechanism initiated by this specific rare variant. Homology modeling suggests that the substitution alters the structural and dynamic properties of the type IV collagen trimer. Genetic analysis comparing members of the 3 families indicated a distant relationship with a shared haplotype, implying a founder effect

Whole Exome Sequencing (WES) revealed underlying complexity in genetic studies of Familial IgA Nephropathy (flgAN)

BACKGROUND: Diagnosis of familial glomerular diseases may be confounded by nonspecific clinical (i.e. hematuria and proteinuria) and/or pathological findings. Indeed, a recent study of familial focal segmental glomerulosclerosis (FSGS) has identified COL4A3 and COL4A4 mutations in ~10% of study families [Kidney Int 86:1253-59, 2014]. In the course of studying a cohort of fIgAN, we unexpectedly identified pathogenic mutations in 13 families with non-IgAN glomerular diseases. METHODS: We performed whole exome sequencing (WES) in 109 patients from 54 families all with at least 2 biopsy-proven cases. RESULTS: Our WES study identified heterozygous/hemizygous pathogenic COL4A3 (c.1504+1G>A; p.G291R; p.G695R; p.G1054E; p.G1286R), COL4A4 (p.Q970X; p.G1508A), and COL4A5 (p.G48R; p.G325R) mutations in 9 families with fIgAN. These mutations occurred at the canonical splice junction or conserved glycine residues and segregated in all affected subjects within family. In two multiplex families, co-existence of thin basement membrane disease (TBMD) with IgAN was also observed in the biopsied subjects in retrospect. Additionally, putative heterozygous pathogenic variants were found in 3 families in the known genes for FSGS (ACTN4, c.398-2A>G), CFHR5 nephropathy (CFHR5, p.C449fs), and membranous nephropathy (PLA2R1, p.C192G) and homozygous mutation in one family in another known gene for FSGS (ADCK4, p.S246N). CONCLUSIONS: The presence of other glomerular diseases may confound the diagnosis of fIgAN in some putatively affected subjects ascertained based on urinary findings or even kidney biopsy. Due to its high prevalence in the general population, TBMD may be an important cause of phenocopy that can confound genetic linkage studies in fIgAN

Disease gene discovery for Familial IgA Nephropathy (FIgAN) by Whole Exome Sequencing (WES)

BACKGROUND: IgAN is the most common primary glomerular disease worldwide. Genome-wide linkage scans have identified multiple susceptibility loci for fIgAN but no disease gene has yet been identified. METHODS: To identify susceptibility genes for fIgAN, we performed WES in 109 patients from 54 families all with >2 biopsy-proven cases and putatively affected members ascertained with persistent hematuria/proteinuria. In 3 multiplex families each with >5 affected cases, we also performed genome-wide linkage scans under a dominant model and focused WES on regions with suggestive linkage. Standard algorithms for sequence alignment, base calling, and QC filtering were applied to identify rare (MAF1 in 3 multiplex families and ~3,000 immunologic candidate genes. We identified 26 candidate genes (i.e. IFIH1, CD33, MSH6, ERAP2, FUT2, MMRN1, MINA, OAS1, TLR1, RNASEL, MARCO, THADA, BTN1A1, PTPRK, RELT, ERCC1, ASB4, LCP1, HK3, ASH1L, LTB, FES, MPO, GP1BA, BACH2, and EMP3), each with rare deleterious variants affecting 2 or 3 unrelated families. CONCLUSIONS: Our results suggest extensive genetic heterogeneity in fIgAN with many disease genes each contributing to a small proportion of cases. Future studies with expanded sample size will aid selection of the most promising candidate genes for functional studies. Identification of disease genes for fIgAN has the potential to improve diagnosis and treatment. Funding: Government Support - Non-U.S