Spanish National Research Council

About: Spanish National Research Council is a government organization based out in Madrid, Spain. It is known for research contribution in the topics: Population & Galaxy. The organization has 79563 authors who have published 220470 publications receiving 7698991 citations. The organization is also known as: CSIC & Consejo Superior de Investigaciones Científicas.

Non-bee insects are important contributors to global crop pollination

Abstract: Wild and managed bees are well documented as effective pollinators of global crops of economic importance. However, the contributions by pollinators other than bees have been little explored despite their potential to contribute to crop production and stability in the face of environmental change. Non-bee pollinators include flies, beetles, moths, butterflies, wasps, ants, birds, and bats, among others. Here we focus on non-bee insects and synthesize 39 field studies from five continents that directly measured the crop pollination services provided by non-bees, honey bees, and other bees to compare the relative contributions of these taxa. Non-bees performed 25–50% of the total number of flower visits. Although non-bees were less effective pollinators than bees per flower visit, they made more visits; thus these two factors compensated for each other, resulting in pollination services rendered by non-bees that were similar to those provided by bees. In the subset of studies that measured fruit set, fruit set increased with non-bee insect visits independently of bee visitation rates, indicating that non-bee insects provide a unique benefit that is not provided by bees. We also show that non-bee insects are not as reliant as bees on the presence of remnant natural or seminatural habitat in the surrounding landscape. These results strongly suggest that non-bee insect pollinators play a significant role in global crop production and respond differently than bees to landscape structure, probably making their crop pollination services more robust to changes in land use. Non-bee insects provide a valuable service and provide potential insurance against bee population declines.

SCF/{beta}-TrCP promotes glycogen synthase kinase 3-dependent degradation of the Nrf2 transcription factor in a Keap1-independent manner.

Abstract: A disadvantage of aerobic life is the constant generation of potentially damaging reactive oxygen species (ROS). The intracellular levels of such species need to be tightly controlled in order to avoid oxidative stress. Transcription factor Nrf2 (NF-E2-related factor 2) plays a critical role in redox homeostasis since it increases the expression of many antioxidant and drug-metabolizing genes, including those encoding heme oxygenase 1 (HO-1), NADPH:quinone oxidoreductase 1, glutathione S-transferases, glutamate-cysteine ligase, and glutathione peroxidases, in response to oxidative and electrophile stressors (13). These genes all contain a common promoter enhancer called the antioxidant response element (ARE) and are transactivated by Nrf2. Because ROS play a role as intracellular signaling molecules for many physiological processes, Nrf2 can have an impact on numerous cell functions, ranging from differentiation and development to proliferation and inflammation. Therefore, Nrf2 activity influences neurodegenerative disease, cardiovascular disease, and cancer (3, 4, 14, 16, 17, 49, 53). While increased Nrf2 transcriptional activity enhances cellular antioxidant defenses and increases the capacity to detoxify drugs, it may also lead to unwanted side effects. For instance, in tumors, high levels of Nrf2 activity have been correlated with a poor prognosis (41). Indeed, high Nrf2 activity has not been favored during evolution (25), but its levels are restricted via both redox-dependent and redox-independent pathways in normal healthy cells (29). In normal cells, Keap1 (Kelch-like ECH-associated protein 1), an E3 ubiquitin ligase substrate adaptor, regulates the level of Nrf2 protein in a redox-dependent fashion (5, 20, 51). The interaction between Nrf2 and Keap1 occurs via a “two-site tethering” process, otherwise called the “hinge and latch” mechanism. In this model, two motifs, a high-affinity ETGE motif and a low-affinity DLG motif, within the N-terminal Neh2 domain of Nrf2 each interact with a separate Kelch repeat domain present in the Keap1 homodimer (40). Both the ETGE motif and the DLG motif are required for the transcription factor to be repressed by Keap1 (28). In addition to its interaction with Nrf2, Keap1 also binds Cullin 3 (Cul3), which forms a core E3 ubiquitin ligase complex through an association with Ring-box1 protein (Rbx1, also called Roc1) (5, 10, 20, 51). The Keap1-Cul3-Rbx1 complex is able to ubiquitinate Nrf2 and target it for proteasomal degradation only under normal redox conditions, and upon exposure to oxidants or electrophiles, Cys-151, Cys-273, and Cys-288 in Keap1 become modified, leading to disturbance of the interaction between Nrf2 and Keap1 (8, 21, 49, 50). Failure of Nrf2 to dock simultaneously onto both Kelch repeat domains enables it to escape ubiquitination by Cul3-Rbx1 (21, 32, 47, 50). Thus, stress-related modification of Keap1 results in Nrf2 stabilization, accumulation of the transcription factor in the nucleus, and upregulation of ARE-driven genes. Perturbation of the Nrf2-Keap1 complex by oxidants and electrophiles is considered the principal mechanism by which Nrf2 accumulates and induces the ARE-gene battery. However, other regulatory mechanisms must exist in order to explain the following: (i) how Nrf2 contributes to the basal expression of certain ARE-driven genes under normal homeostatic conditions, (ii) how Nrf2 activity returns to its low basal levels after the intracellular redox balance has been restored, and (iii) how Nrf2 activity is limited during oxidative and electrophile stress. Conventional cell signaling studies have suggested that Nrf2 might be regulated by protein phosphorylation (2, 6, 15, 18, 36, 44). Previously, we presented data suggesting that GSK-3β (glycogen synthase kinase 3β) influences the nuclear exclusion and inactivation of Nrf2 (37-39). However, the mechanistic connection between GSK-3 and Nrf2 remains largely unexplored. A number of studies have demonstrated that GSK-3 directs the ubiquitination and proteasomal degradation of various transcription factors and other proteins by SCF/β-TrCP; these include Snail (54), β-catenin (1, 22, 34), Gli2 and Gli3 (33, 48), Xom (55), Cdc 25a (19), FGD1 and -3 (11, 12), Mcl-1 (7), securin (24), prolactin receptor (46), and the phosphatase PHLPP1 (23). In these instances, GSK-3 phosphorylates a cluster of Ser/Thr residues in target proteins, which are then recognized by SCF/β-TrCP. In turn, the complex formed by SCF/β-TrCP binds the Cullin-1 (Cul1) scaffold protein to form a complete E3 ligase by association with a linker protein called Skp1 and with Rbx1. Therefore, β-TrCP is an adapter protein that contains a Skp1-binding site called F-box and a WD recognition domain for phosphorylated substrates in the consensus motif DpSGX(1-4)pS (9, 42). To date, the existence of a phosphodegron in Nrf2 has not been explored. In the present article, we report that Nrf2 is destabilized as a consequence of its phosphorylation by GSK-3 and subsequent ubiquitination by SCF/β-TrCP. This pathway represents an alternative mechanism to the Keap1-dependent degradation of Nrf2 and provides a means by which this transcription factor can be regulated in a redox-independent manner.

Disrupted cardiac development but normal hematopoiesis in mice deficient in the second CXCL12/SDF-1 receptor, CXCR7

Abstract: Chemotactic cytokines (chemokines) attract immune cells, although their original evolutionary role may relate more closely with embryonic development. We noted differential expression of the chemokine receptor CXCR7 (RDC-1) on marginal zone B cells, a cell type associated with autoimmune diseases. We generated Cxcr7−/− mice but found that CXCR7 deficiency had little effect on B cell composition. However, most Cxcr7−/− mice died at birth with ventricular septal defects and semilunar heart valve malformation. Conditional deletion of Cxcr7 in endothelium, using Tie2-Cre transgenic mice, recapitulated this phenotype. Gene profiling of Cxcr7−/− heart valve leaflets revealed a defect in the expression of factors essential for valve formation, vessel protection, or endothelial cell growth and survival. We confirmed that the principal chemokine ligand for CXCR7 was CXCL12/SDF-1, which also binds CXCR4. CXCL12 did not induce signaling through CXCR7; however, CXCR7 formed functional heterodimers with CXCR4 and enhanced CXCL12-induced signaling. Our results reveal a specialized role for CXCR7 in endothelial biology and valve development and highlight the distinct developmental role of evolutionary conserved chemokine receptors such as CXCR7 and CXCR4.

Plant functional traits have globally consistent effects on competition

Abstract: Phenotypic traits and their associated trade-offs have been shown to have globally consistent effects on individual plant physiological functions, but how these effects scale up to influence competition, a key driver of community assembly in terrestrial vegetation, has remained unclear. Here we use growth data from more than 3 million trees in over 140,000 plots across the world to show how three key functional traits--wood density, specific leaf area and maximum height--consistently influence competitive interactions. Fast maximum growth of a species was correlated negatively with its wood density in all biomes, and positively with its specific leaf area in most biomes. Low wood density was also correlated with a low ability to tolerate competition and a low competitive effect on neighbours, while high specific leaf area was correlated with a low competitive effect. Thus, traits generate trade-offs between performance with competition versus performance without competition, a fundamental ingredient in the classical hypothesis that the coexistence of plant species is enabled via differentiation in their successional strategies. Competition within species was stronger than between species, but an increase in trait dissimilarity between species had little influence in weakening competition. No benefit of dissimilarity was detected for specific leaf area or wood density, and only a weak benefit for maximum height. Our trait-based approach to modelling competition makes generalization possible across the forest ecosystems of the world and their highly diverse species composition.