Do provisioning ecosystem services change along gradients of increasing agricultural production?

Context: Increasing agricultural production shapes the flow of ecosystem services (ES), including provisioning services that support the livelihoods and nutrition of people in tropical developing countries. Although our broad understanding of the social-ecological consequences of agricultural intensification is growing, how it impacts provisioning ES is still unknown. Objectives: We examined the household use of provisioning ES across a gradient of increasing agricultural production in seven tropical countries (Bangladesh, Burkina Faso, Cameroon, Ethiopia, Indonesia, Nicaragua and Zambia). We answered two overarching questions: (1) does the use of provisioning ES differ along gradients of agriculture production ranging from zones of subsistence to moderate and to high agriculture production? and (2) are there synergies and/or trade-offs within and among groups of ES within these zones? Methods: Using structured surveys, we asked 1900 households about their assets, livestock, crops, and collection of forest products. These questions allowed us to assess the number of provisioning ES households used, and whether the ES used are functionally substitutable (i.e., used similarly for nutrition, material, and energy). Finally, we explored synergies and trade-offs among household use of provisioning ES. Results: As agricultural production increased, provisioning ES declined both in total number and in different functional groups used. We found more severe decreases in ES for relatively poorer households. Within the functional groups of ES, synergistic relationships were more often found than trade-offs in all zones, including significant synergies among livestock products (dairy, eggs, meat) and fruits. Conclusions: Considering landscape context provides opportunities to enhance synergies among provisioning services for households, supporting resilient food systems and human well-being

Ant-aphid mutualism: How do ants find aphids?

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Mapping of the gene for the p60 subunit of the human chromatin assembly factor (CAF1A) to the Down syndrome region of chromosome 21

Exon trapping was used to clone portions of genes from the Down syndrome critical region (DSCR) of human chromosome 21. One trapped sequence showed complete homology with nucleotide sequence U20980 (GenBank), which corresponds to the gene for the p60 subunit of the human chromatin assembly factor-1 (CAF1A). We mapped this gene to human chromosome 21 by fluorescence in situ hybridization, by the use of somatic cell hybrids, and by hybridization to chromosome 21-specific YACs and cosmids. The CAF1A gene localizes to YACs 745H11 and 230E8 of the Chumakov et al. (1992, Nature 359: 380) YAC contig, within the DSCR on 21q22. This CAF1A, which belongs to the WD-motif family of genes and interacts with other polypeptide subunits to promote assembly of histones to replicating DNA, may contribute in a gene dosage-dependent manner to the phenotype of Down syndrome

Ant-aphid mutualism: A question of microorganisms ?

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The complex SNP and CNV genetic architecture of the increased risk of congenital heart defects in Down syndrome

Congenital heart defect (CHD) occurs in 40% of Down syndrome (DS) cases. While carrying three copies of chromosome 21 increases the risk for CHD, trisomy 21 itself is not sufficient to cause CHD. Thus, additional genetic variation and/or environmental factors could contribute to the CHD risk. Here we report genomic variations that in concert with trisomy 21, determine the risk for CHD in DS. This case-control GWAS includes 187 DS with CHD (AVSD = 69, ASD = 53, VSD = 65) as cases, and 151 DS without CHD as controls. Chromosome 21–specific association studies revealed rs2832616 and rs1943950 as CHD risk alleles (adjusted genotypic P-values <0.05). These signals were confirmed in a replication cohort of 92 DS-CHD cases and 80 DS-without CHD (nominal P-value 0.0022). Furthermore, CNV analyses using a customized chromosome 21 aCGH of 135K probes in 55 DS-AVSD and 53 DS-without CHD revealed three CNV regions associated with AVSD risk (FDR ≤ 0.05). Two of these regions that are located within the previously identified CHD region on chromosome 21 were further confirmed in a replication study of 49 DS-AVSD and 45 DS- without CHD (FDR ≤ 0.05). One of these CNVs maps near the RIPK4 gene, and the second includes the ZBTB21 (previously ZNF295) gene, highlighting the potential role of these genes in the pathogenesis of CHD in DS. We propose that the genetic architecture of the CHD risk of DS is complex and includes trisomy 21, and SNP and CNV variations in chromosome 21. In addition, a yet-unidentified genetic variation in the rest of the genome may contribute to this complex genetic architecture.The study was supported by grants from the NCCR–Frontiers in Genetics, the European AnEuploidy project, the Fondation Child Care, the SNF 144082, the ERC 249968 to S.E.A., and the Spanish Ministry of Ecomomy and Competitivity to X.E. P.M. was supported by a grant from the Bodossaki foundation. K.P. was supported by the EMBO long-term fellowship program ALTF 527-201