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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Thomas Arbogast; Abdel-Mouttalib Ouagazzal; Claire Chevalier; Maksym V. Kopanitsa; +7 Authors

    The 16p11.2 600 kb BP4-BP5 deletion and duplication syndromes have been associated with developmental delay; autism spectrum disorders; and reciprocal effects on the body mass index, head circumference and brain volumes. Here, we explored these relationships using novel engineered mouse models carrying a deletion (Del/+) or a duplication (Dup/+) of the Sult1a1-Spn region homologous to the human 16p11.2 BP4-BP5 locus. On a C57BL/6N inbred genetic background, Del/+ mice exhibited reduced weight and impaired adipogenesis, hyperactivity, repetitive behaviors, and recognition memory deficits. In contrast, Dup/+ mice showed largely opposite phenotypes. On a F1 C57BL/6N × C3B hybrid genetic background, we also observed alterations in social interaction in the Del/+ and the Dup/+ animals, with other robust phenotypes affecting recognition memory and weight. To explore the dosage effect of the 16p11.2 genes on metabolism, Del/+ and Dup/+ models were challenged with high fat and high sugar diet, which revealed opposite energy imbalance. Transcriptomic analysis revealed that the majority of the genes located in the Sult1a1-Spn region were sensitive to dosage with a major effect on several pathways associated with neurocognitive and metabolic phenotypes. Whereas the behavioral consequence of the 16p11 region genetic dosage was similar in mice and humans with activity and memory alterations, the metabolic defects were opposite: adult Del/+ mice are lean in comparison to the human obese phenotype and the Dup/+ mice are overweight in comparison to the human underweight phenotype. Together, these data indicate that the dosage imbalance at the 16p11.2 locus perturbs the expression of modifiers outside the CNV that can modulate the penetrance, expressivity and direction of effects in both humans and mice. Author Summary The 16p11.2 BP4-BP5 deletion and duplication syndromes are frequent copy number variants in humans, and are associated with developmental delay and autism spectrum disorders, with a reciprocal effect on head circumference and body mass index. Here we explored gene dosage effect in mouse models and found that the deletion and duplication induced opposite behavioral phenotypes. Notably, we observed that some behavioral phenotypes, such as social interaction, were sensitive to the genetic background. For the metabolism, the energy imbalance and adipocyte phenotypes were mirrored in the deletion and duplication carriers but opposite to the human phenotypes, the deletion mouse carriers were lean whereas the individuals with the deletion were obese. The main cause of the phenotypic features is the copy number variation of the 16p11.2 region with many genetic pathways altered in the striatum and the liver. Thus the final consequences of the rearrangement are likely governed by the interplay between many cellular pathways in both human cases and mouse models.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Europe PubMed Centra...arrow_drop_down
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    Other literature type . 2016
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    PLoS Genetics
    Article . 2016 . Peer-reviewed
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    PLoS Genetics
    Article . 2016
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Europe PubMed Centra...arrow_drop_down
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      Other literature type . 2016
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      PLoS Genetics
      Article . 2016 . Peer-reviewed
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      PLoS Genetics
      Article . 2016
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      PLoS Genetics
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Patricia Blanchet; Martina Bebin; Shaam Bruet; Gregory M Cooper; +15 Authors

    Deletions at chromosome 2p25.3 are associated with a syndrome consisting of intellectual disability and obesity. The smallest region of overlap for deletions at 2p25.3 contains PXDN and MYT1L. MYT1L is expressed only within the brain in humans. We hypothesized that single nucleotide variants (SNVs) in MYT1L would cause a phenotype resembling deletion at 2p25.3. To examine this we sought MYT1L SNVs in exome sequencing data from 4, 296 parent-child trios. Further variants were identified through a genematcher-facilitated collaboration. We report 9 patients with MYT1L SNVs (4 loss of function and 5 missense). The phenotype of SNV carriers overlapped with that of 2p25.3 deletion carriers. To identify the transcriptomic consequences of MYT1L loss of function we used CRISPR-Cas9 to create a knockout cell line. Gene Ontology analysis in knockout cells demonstrated altered expression of genes that regulate gene expression and that are localized to the nucleus. These differentially expressed genes were enriched for OMIM disease ontology terms “mental retardation”. To study the developmental effects of MYT1L loss of function we created a zebrafish knockdown using morpholinos. Knockdown zebrafish manifested loss of oxytocin expression in the preoptic neuroendocrine area. This study demonstrates that MYT1L variants are associated with syndromic obesity in humans. The mechanism is related to dysregulated expression of neurodevelopmental genes and altered development of the neuroendocrine hypothalamus. Author summary Intellectual disability is defined by having an intelligence quotient of less than 70 points, and it affects about 2–3 people in every 100. Obesity is defined as having a body mass index of over 30 in adults or over the 95th centile in children. Both of these conditions are major public health concerns in Western countries. Genetic studies have shown that small missing pieces of chromosome (deletions, which remove many genes) and changes to the lettering of genes (which stop the gene from working, mutations) can cause intellectual disability or obesity. Here we identified 9 children with intellectual disability and obesity who have mutations in a gene called MYT1L. This gene is thought to give an important instruction for brain development. To find out what the effect of loss of MYT1L is on brain development we reduced the levels of MYT1L (using a special chemical) in an experimental zebrafish. This showed that loss of MYT1L in zebrafish causes a problem with the development of the hypothalamus, which may explain how MYT1L mutations cause obesity in humans. In the zebrafish there was also reduction of a brain hormone called oxytocin which is involved in thought processes, which may explain why MYT1L mutations cause intellectual disability. We have identified a new genetic condition caused by MYT1L mutations, further study of this gene will help us understand, and treat, intellectual disability and obesity.

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    PLoS Genetics
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    PLoS Genetics
    Article . 2017 . Peer-reviewed
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    PLoS Genetics
    Article . 2017
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Europe PubMed Centra...arrow_drop_down
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      PLoS Genetics
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      PLoS Genetics
      Article . 2017 . Peer-reviewed
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      PLoS Genetics
      Article . 2017
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    Authors: William A, Banks;

    The blood–brain barrier (BBB) regulates the blood‐to‐brain passage of gastrointestinal hormones, thus informing the brain about feeding and nutritional status. Disruption of this communication results in dysregulation of feeding and body weight control. Leptin, which crosses the BBB to inform the CNS about adiposity, provides an example. Impaired leptin transport, especially coupled with central resistance, results in obesity. Various substances/conditions regulate leptin BBB transport. For example, triglycerides inhibit leptin transport. This may represent an evolutionary adaptation in that hypertriglyceridemia occurs during starvation. Inhibition of leptin, an anorectic, during starvation could have survival advantages. The large number of other substances that influence feeding is explained by the complexity of feeding. This complexity includes cognitive aspects; animals in the wild are faced with cost/benefit analyses to feed in the safest, most economical way. This cognitive aspect partially explains why so many feeding substances affect neurogenesis, neuroprotection, and cognition. The relation between triglycerides and cognition may be partially mediated through triglyceride's ability to regulate the BBB transport of cognitively active gastrointestinal hormones such as leptin, insulin, and ghrelin.

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    Annals of the New York Academy of Sciences
    Article . 2012 . Peer-reviewed
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      Annals of the New York Academy of Sciences
      Article . 2012 . Peer-reviewed
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    Authors: Shan, Luo; Sydney G, O'Connor; Britni R, Belcher; Kathleen A, Page;

    ObjectivePhysical activity (PA) promotes weight maintenance, potentially because of its beneficial effects on feeding behavior regulation via diminished food cue reactivity within brain reward regions. This study examined how levels of PA and sedentary behavior (SB) relate to brain responses to food cues.MethodsParticipants (22 lean, 18 with obesity) completed three to five PA recalls over 2 months. Average minutes per day of moderate to vigorous PA (MVPA) and SB were calculated. Participants completed a functional magnetic resonance imaging session, viewing food and nonfood images following glucose ingestion. Region of interest (ROI) analysis examined associations between MVPA and brain percent signal change in response to food versus nonfood images, controlling for obesity and sex. Secondary analysis examined associations between SB and brain responses to food cues.ResultsGreater MVPA was associated with decreased food cue reactivity after glucose across brain ROIs (β = −0.00057, P = 0.005), controlling for obesity and sex. Greater SB was associated with increased food cue reactivity after glucose across brain ROIs in unadjusted analyses (β = 0.00041, P = 0.026).ConclusionsPA may have beneficial effects on brain regulation of feeding behavior after caloric intake in lean individuals and individuals with obesity.

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    Obesity
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    Obesity
    Article . 2018 . Peer-reviewed
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      Obesity
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      Obesity
      Article . 2018 . Peer-reviewed
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    Authors: Imdorf, Anton; Bogdanov, Stefan; Ibáñez Ochoa, Rubén; W. Calderone, Nicholas;

    soni, parasite des colonies d'abeilles. Le developpement de la resistance des populations de Varroa jacobsoni et le spectre de la contamination des produits du rucher ont fortement stimule la mise au point de nouvelles strategies de traitement qui diminuent la possibilite d'un developpement rapide de la resistance et l'accumulation de residus. Cet article passe en revue l'utilisation des huiles essentielles (h.e.) et de leurs composants dans la lutte contre V. jacobsoni. « Huiles essentielles » est un terme generique qui designe les composants liquides et hautement volatiles des plantes, marques par une odeur forte et caracteristique. Les terpenes (principalement les monoterpenes) representent la majeure partie (environ 90 %) de ces composants. L'eucalyptol, le camphre, le-menthol et le thymol sont des monoterpenes typiques. Chaque espece de plante tend a avoir une composition en h.e. unique. Pourtant, certaines especes ont des varietes denommees chemotypes, dont la composition en h.e. varie. On a utilise les methodes de criblage au laboratoire pour tester sur V. jacobsoni et sur les abeilles la toxicite, la repulsivite, l'attractivite, ainsi que les effets sur la reproduction, des h.e. et de leurs composants. Au total, c'est plus de 150 h.e. et composants d'h.e. qui ont ete testes (tableaux I-III), mais peu d'entre eux se sont montres efficaces lors de leur utilisation sur ruches en conditions de terrain. Une variation enorme des conditions du milieu local et des colonies, ainsi que la difficulte d'obtenir des h.e. standardisees, rendent difficile la prevision du resultat des nombreux traitements. Les residus dans le miel peuvent conduire a des effets negatifs sur le gout. L'analyse quantitative des residus est exigee pour l'enregistrement du produit. La nature complexe de beaucoup d'h.e. et le fait que de nombreux composants des h.e. sont presents a l'etat naturel dans le miel font que l'analyse des residus est difficile. Neanmoins ces difficultes disparaissent lorsqu'on utilise individuellement les composants des h.e. La plupart sont volatils et disponibles sur le marche a prix raisonnables. Parmi tous les composants testes des h.e., c'est le thymol qui a eu le meilleur resultat en apiculture pratique, Dans les essais en champ le thymol pur (tableau IV) et les melanges a base de thymol (tableau V) ont montre une activite varroacide elevee. Le thymol est bien tolere par les abeilles. Si les traitements sont effectues en dehors de la periode de miellee, les residus de thymol dans le miel n'augmentent pas lorsqu'on multiplie les traitements et restent sous le seuil de detection gustative, qui se situe entre 1,1 et 1,6 mg.kg -1 . Selon les etudes on a trouve iles residus compris entre 0,02 et 0,48 mg.kg -1 . Mais les traitements au thymol pendant la miellee peuvent conduire a des residus plus eleves qui modifient le gout du miel. Le thymol, de meme que d'autres monoterpenes tels que le menthol et le camphre, ont le statut GRAS (generally recognized as safe, generalement reconnu comme sans danger), de la FAO aux concentrations allant jusqu'a 50 mg.kg -1 . Les residus de ces substances dans le miel ne posent donc pas de probleme toxicologique. Apres un traitement au thymol les residus dans la cire sont 1 000 fois plus eleves que dans le miel, mais ils diminuent rapidement par evaporation des que le traitement est arrete.

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    Apidologie
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    Other literature type . 1999
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    Other literature type . 1999
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    Apidologie
    Article . 1999 . Peer-reviewed
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      Other literature type . 1999
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      Apidologie
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    Authors: Franklin, J; Andrade, R; Daniels, ML; Fairbairn, P; +19 Authors

    AbstractAimSeasonally dry tropical forest (SDTF) of the Caribbean Islands (primarily West Indies) is floristically distinct from Neotropical SDTF in Central and South America. We evaluate whether tree species composition was associated with climatic gradients or geographical distance. Turnover (dissimilarity) in species composition of different islands or among more distant sites would suggest communities structured by speciation and dispersal limitations. A nested pattern would be consistent with a steep resource gradient. Correlation of species composition with climatic variation would suggest communities structured by broad‐scale environmental filtering.LocationThe West Indies (The Bahamas, Cuba, Hispaniola, Jamaica, Puerto Rico, US Virgin Islands, Guadeloupe, Martinique, St. Lucia), Providencia (Colombia), south Florida (USA) and Florida Keys (USA).TaxonSeed plants—woody taxa (primarily trees).MethodsWe compiled 572 plots from 23 surveys conducted between 1969 and 2016. Hierarchical clustering of species in plots, and indicator species analysis for the resulting groups of sites, identified geographical patterns of turnover in species composition. Nonparametric analysis of variance, applied to principal components of bioclimatic variables, determined the degree of covariation in climate with location. Nestedness versus turnover in species composition was evaluated using beta diversity partitioning. Generalized dissimilarity modelling partitioned the effect of climate versus geographical distance on species composition.ResultsDespite a set of commonly occurring species, SDTF tree community composition was distinct among islands and was characterized by spatial turnover on climatic gradients that covaried with geographical gradients. Greater Antillean islands were characterized by endemic indicator species. Northern subtropical areas supported distinct, rather than nested, SDTF communities in spite of low levels of endemism.Main conclusionsThe SDTF species composition was correlated with climatic variation. SDTF on large Greater Antillean islands (Hispaniola, Jamaica and Cuba) was characterized by endemic species, consistent with their geological history and the biogeography of plant lineages. These results suggest that both environmental filtering and speciation shape Caribbean SDTF tree communities.

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    Apollo
    Article . 2018
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    Apollo
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    Journal of Biogeography
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    Journal of Biogeography
    Article . 2018 . Peer-reviewed
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      Journal of Biogeography
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    Authors: Jia Yao; Shuhua Chen; Zisu Mao; Enrique Cadenas; +1 Authors

    Previously, we demonstrated that mitochondrial bioenergetic deficits preceded Alzheimer's disease (AD) pathology in the female triple-transgenic AD (3xTgAD) mouse model. In parallel, 3xTgAD mice exhibited elevated expression of ketogenic markers, indicating a compensatory mechanism for energy production in brain. This compensatory response to generate an alternative fuel source was temporary and diminished with disease progression. To determine whether this compensatory alternative fuel system could be sustained, we investigated the impact of 2-deoxy-D-glucose (2-DG), a compound known to induce ketogenesis, on bioenergetic function and AD pathology burden in brain. 6-month-old female 3xTgAD mice were fed either a regular diet (AIN-93G) or a diet containing 0.04% 2-DG for 7 weeks. 2-DG diet significantly increased serum ketone body level and brain expression of enzymes required for ketone body metabolism. The 2-DG-induced maintenance of mitochondrial bioenergetics was paralleled by simultaneous reduction in oxidative stress. Further, 2-DG treated mice exhibited a significant reduction of both amyloid precursor protein (APP) and amyloid beta (Aβ) oligomers, which was paralleled by significantly increased α-secretase and decreased γ-secretase expression, indicating that 2-DG induced a shift towards a non-amyloidogenic pathway. In addition, 2-DG increased expression of genes involved in Aβ clearance pathways, degradation, sequestering, and transport. Concomitant with increased bioenergetic capacity and reduced β-amyloid burden, 2-DG significantly increased expression of neurotrophic growth factors, BDNF and NGF. Results of these analyses demonstrate that dietary 2-DG treatment increased ketogenesis and ketone metabolism, enhanced mitochondrial bioenergetic capacity, reduced β-amyloid generation and increased mechanisms of β-amyloid clearance. Further, these data link bioenergetic capacity with β-amyloid generation and demonstrate that β-amyloid burden was dynamic and reversible, as 2-DG reduced activation of the amyloidogenic pathway and increased mechanisms of β-amyloid clearance. Collectively, these data provide preclinical evidence for dietary 2-DG as a disease-modifying intervention to delay progression of bioenergetic deficits in brain and associated β-amyloid burden.

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    PLoS ONE
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    PLoS ONE
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    Authors: Sun Hee Yim; Clary B. Clish; Vadim N. Gladyshev;

    SUMMARY Selenium (Se) is an essential trace element because of its presence in selenoproteins in the form of selenocysteine residue. Both Se deficiency, which compromises selenoprotein functions, and excess Se, which is toxic, have been associated with altered redox homeostasis and adverse health conditions. Surprisingly, we found that, although Se deficiency led to a drastic decline in selenoprotein expression, mice subjected to this dietary regimen for their entire life had normal lifespans. To understand the molecular mechanisms involved, we performed systemic analyses at the level of metabolome, transcriptome, and microRNA profiling. These analyses revealed that Se deficiency reduced amino acid levels, elevated mononucleotides, altered metabolism, and activated signaling pathways linked to longevity-related nutrient sensing. The data show that the metabolic control associated with nutrient sensing coordinately responds to suppressed selenoprotein functions, resulting in normal lifespan under Se deficiency. In Brief Yim et al. report that selenium deficiency in mice is associated with pro-longevity mechanisms because of reduced amino acid levels and altered nutrient signaling. Graphical Abstract

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    Authors: Niu, Kechang; Schmid, Bernhard; Choler, Philippe; Du, Guozhen;

    BackgroundUnderstanding the relationship between species traits and species abundance is an important goal in ecology and biodiversity science. Although theoretical studies predict that traits related to performance (e.g. reproductive allocation) are most directly linked to species abundance within a community, empirical investigations have rarely been done. It also remains unclear how environmental factors such as grazing or fertilizer application affect the predicted relationship.MethodologyWe conducted a 3-year field experiment in a Tibetan alpine meadow to assess the relationship between plant reproductive allocation (RA) and species relative abundance (SRA) on control, grazed and fertilized plots. Overall, the studied plant community contained 32 common species.Principal findingsAt the treatment level, (i) RA was negatively correlated with SRA on control plots and during the first year on fertilized plots. (ii) No negative RA-SRA correlations were observed on grazed plots and during the second and third year on fertilized plots. (iii) Seed size was positively correlated with SRA on control plots. At the plot level, the correlation between SRA and RA were not affected by treatment, year or species composition.Conclusions/significanceOur study shows that the performance-related trait RA can negatively affect SRA within communities, which is possibly due to the tradeoffs between clonal growth (for space occupancy) and sexual reproduction. We propose that if different species occupy different positions along these tradeoffs it will contribute to biodiversity maintenance in local communities or even at lager scale.

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    Authors: Poussin, Jean-Christophe; Diallo, Youssouf; Legoupil, Jean-Claude; Sow, Abdoulaye;

    International audience; Village irrigation schemes cover about 25% of the irrigated area on the two banks of the Senegal River. We analyzed irrigation scheme and rice crop management practices during the 1998 wet season in this type of irrigation scheme in Mauritania. Average yield was 4.8 t ha-1; problems with irrigation rules resulted in great variability of irrigation frequency between fields, and sub-optimal timing of nitrogen fertilizer application resulted in yield losses. Based on this diagnosis, we suggested to farmers new irrigation rules and cropping calendars planned on the scale of the irrigation scheme. Planned cropping calendars were built using CalCul, a software that we designed on the basis of the irrigated rice development model RIDEV. These suggestions of improved collective management were implemented in the 1999 and 2000 wet seasons. Average yield reached 7.2 t ha-1 in 1999 and 8.2 t ha-1 in 2000, without any significant increase in production costs. This great increase in rice productivity was mainly due to better collective management obtained through planning cropping calendars. This result showed that technical innovation is not the only way to improve productivity.

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    Agronomy for Sustainable Development
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    Authors: Thomas Arbogast; Abdel-Mouttalib Ouagazzal; Claire Chevalier; Maksym V. Kopanitsa; +7 Authors

    The 16p11.2 600 kb BP4-BP5 deletion and duplication syndromes have been associated with developmental delay; autism spectrum disorders; and reciprocal effects on the body mass index, head circumference and brain volumes. Here, we explored these relationships using novel engineered mouse models carrying a deletion (Del/+) or a duplication (Dup/+) of the Sult1a1-Spn region homologous to the human 16p11.2 BP4-BP5 locus. On a C57BL/6N inbred genetic background, Del/+ mice exhibited reduced weight and impaired adipogenesis, hyperactivity, repetitive behaviors, and recognition memory deficits. In contrast, Dup/+ mice showed largely opposite phenotypes. On a F1 C57BL/6N × C3B hybrid genetic background, we also observed alterations in social interaction in the Del/+ and the Dup/+ animals, with other robust phenotypes affecting recognition memory and weight. To explore the dosage effect of the 16p11.2 genes on metabolism, Del/+ and Dup/+ models were challenged with high fat and high sugar diet, which revealed opposite energy imbalance. Transcriptomic analysis revealed that the majority of the genes located in the Sult1a1-Spn region were sensitive to dosage with a major effect on several pathways associated with neurocognitive and metabolic phenotypes. Whereas the behavioral consequence of the 16p11 region genetic dosage was similar in mice and humans with activity and memory alterations, the metabolic defects were opposite: adult Del/+ mice are lean in comparison to the human obese phenotype and the Dup/+ mice are overweight in comparison to the human underweight phenotype. Together, these data indicate that the dosage imbalance at the 16p11.2 locus perturbs the expression of modifiers outside the CNV that can modulate the penetrance, expressivity and direction of effects in both humans and mice. Author Summary The 16p11.2 BP4-BP5 deletion and duplication syndromes are frequent copy number variants in humans, and are associated with developmental delay and autism spectrum disorders, with a reciprocal effect on head circumference and body mass index. Here we explored gene dosage effect in mouse models and found that the deletion and duplication induced opposite behavioral phenotypes. Notably, we observed that some behavioral phenotypes, such as social interaction, were sensitive to the genetic background. For the metabolism, the energy imbalance and adipocyte phenotypes were mirrored in the deletion and duplication carriers but opposite to the human phenotypes, the deletion mouse carriers were lean whereas the individuals with the deletion were obese. The main cause of the phenotypic features is the copy number variation of the 16p11.2 region with many genetic pathways altered in the striatum and the liver. Thus the final consequences of the rearrangement are likely governed by the interplay between many cellular pathways in both human cases and mouse models.

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    PLoS Genetics
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