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In sea cage fish farming, production quotas aim to constrain the impact of fish farming on the surrounding ecosystem. It is unknown how these quotas affect economic profitability and environmental impact of genetic improvement. We combined bioeconomic modelling with life cycle assessment (LCA) to calculate the economic (EV) and environmental (ENV) values of thermal growth coefficient (TGC) and feed conversion ratio (FCR) of sea bass reared in sea cages, given four types of quota commonly used in Europe: annual production (Qprod), annual feed distributed (Qannual_ feed), standing stock (Qstock), and daily feed distributed (Qdaily_ feed). ENV were calculated for LCA impact categories climate change, eutrophication and acidification. ENV were expressed per ton of fish produced per year (ENV(fish)) and per farm per year (ENV(farm)). Results show that irrespective of quota used, EV of FCR as well as ENV(fish) and ENV(farm) were always positive, meaning that improving FCR increased profit and decreased environmental impacts. However, the EV and the ENV(fish) of TGC were positive only when quota was Qstock or Qdaily_ feed. Moreover, the ENV(farm) of TGC was negative in Qstock and Qdaily_ feed quotas, meaning that improving TGC increased the environmental impact of the farm. We conclude that Qstock quota and Qdaily_ feed quota are economically favorable to a genetic improvement of TGC, a major trait for farmers. However, improving TGC increases the environmental impact of the farm. Improving FCR represents a good opportunity to balance out this increase but more information on its genetic background is needed to develop breeding programs improving FCR.

Soil-borne vascular wilt diseases caused by Verticillium spp. are among the most destructive diseases worldwide in a wide range of plant species. The most effective means of controlling Verticillium wilt diseases is the use of genetic resistance. We have previously reported the identification of four activation-tagged Arabidopsis mutants which showed enhanced resistance to Verticillium wilt. Among these, one mutant also showed enhanced resistance to Ralstonia solanacearum, a bacterial vascular wilt pathogen. Cloning of the activation tag revealed an insertion upstream of gene At3g13437, which we designated as EWR1 (for Enhancer of vascular Wilt Resistance 1) that encodes a putatively secreted protein of unknown function. The search for homologs of Arabidopsis EWR1 (AtEWR1) in public databases only identified homologs within the Brassicaceae family. We subsequently cloned the EWR1 homolog from Brassica oleracea (BoEWR1) and show that over-expression in Arabidopsis results in V. dahliae resistance. Moreover, over-expression of AtEWR1 and BoEWR1 in N. benthamiana, a member of the Solanaceae family, results in V. dahliae resistance, suggesting that EWR1 homologs can be used to engineer Verticillium wilt resistance in non-Brassicaceae crops as well.

Meiosis is a specialized eukaryotic cell division that generates haploid gametes required for sexual reproduction. During meiosis, homologous chromosomes pair and undergo reciprocal genetic exchange, termed crossover (CO). Meiotic CO frequency varies along the physical length of chromosomes and is determined by hierarchical mechanisms, including epigenetic organization, for example methylation of the DNA and histones. Here we investigate the role of DNA methylation in determining patterns of CO frequency along Arabidopsis thaliana chromosomes. In A. thaliana the pericentromeric regions are repetitive, densely DNA methylated, and suppressed for both RNA polymerase-II transcription and CO frequency. DNA hypomethylated methyltransferase1 (met1) mutants show transcriptional reactivation of repetitive sequences in the pericentromeres, which we demonstrate is coupled to extensive remodeling of CO frequency. We observe elevated centromere-proximal COs in met1, coincident with pericentromeric decreases and distal increases. Importantly, total numbers of CO events are similar between wild type and met1, suggesting a role for interference and homeostasis in CO remodeling. To understand recombination distributions at a finer scale we generated CO frequency maps close to the telomere of chromosome 3 in wild type and demonstrate an elevated recombination topology in met1. Using a pollen-typing strategy we have identified an intergenic nucleosome-free CO hotspot 3a, and we demonstrate that it undergoes increased recombination activity in met1. We hypothesize that modulation of 3a activity is caused by CO remodeling driven by elevated centromeric COs. These data demonstrate how regional epigenetic organization can pattern recombination frequency along eukaryotic chromosomes., Author Summary The majority of eukaryotes reproduce via a specialized cell division called meiosis, which generates gametes with half the number of chromosomes. During meiosis, homologous chromosomes pair and undergo a process of reciprocal exchange, called crossing-over (CO), which generates new combinations of genetic variation. The relative chance of a CO occurring is variable along the chromosome, for example COs are suppressed in the centromeric regions that attach to the spindle during chromosome segregation. These patterns correlate with domains of epigenetic organization along chromosomes, including methylation of the DNA and histones. DNA methylation occurs most densely in the centromeric regions of Arabidopsis thaliana chromosomes, where it is required for transcriptional suppression of repeated sequences. We demonstrate that mutants that lose DNA methylation (met1) show epigenetic remodeling of crossover frequencies, with increases in the centromeric regions and compensatory changes in the chromosome arms, though the total number of crossovers remains the same. As crossover numbers and distributions are subject to homeostatic mechanisms, we propose that these drive crossover remodeling in met1 in response to epigenetic change in the centromeric regions. Together these data demonstrate how domains of epigenetic organization are important for shaping patterns of crossover frequency along eukaryotic chromosomes.

Chantier qualité GA; We characterized a new quorum-sensing regulator, PlcRa, which is present in various members of the B. cereus group and identified a signaling heptapeptide for PlcRa activity: PapRa(7). We demonstrated that PlcRa is a 3D structural paralog of PlcR using sequence analysis and homology modeling. A comparison of the transcriptomes at the onset of stationary phase of a ΔplcRa mutant and the wild-type B. cereus ATCC 14579 strain showed that 68 genes were upregulated and 49 genes were downregulated in the ΔplcRa mutant strain (>3-fold change). Genes involved in the cysteine metabolism (putative CymR regulon) were downregulated in the ΔplcRa mutant strain. We focused on the gene with the largest difference in expression level between the two conditions, which encoded -AbrB2- a new regulator of the AbrB family. We demonstrated that purified PlcRa bound specifically to the abrB2 promoter in the presence of synthetic PapRa(7), in an electrophoretic mobility shift assay. We further showed that the AbrB2 regulator controlled the expression of the yrrT operon involved in methionine to cysteine conversion. We found that the ΔplcRa mutant strain was more sensitive to hydrogen peroxide- and disulfide-induced stresses than the wild type. When cystine was added to the culture of the ΔplcRa mutant, challenged with hydrogen peroxide, growth inhibition was abolished. In conclusion, we identified a new RNPP transcriptional regulator in B. cereus that activated the oxidative stress response and cysteine metabolism in transition state cells.

Background and Aims: High protein (HP) diets are suggested to positively modulate obesity and associated increased prevalence of non-alcoholic fatty liver (NAFLD) disease in humans and rodents. The aim of our study was to detect mechanisms by which a HP diet affects hepatic lipid accumulation. [br/] Methods: To investigate the acute and long term effect of high protein ingestion on hepatic lipid accumulation under both low and high fat (HF) conditions, mice were fed combinations of high (35 energy%) or low (10 energy%) fat and high (50 energy%) or normal (15 energy%) protein diets for 1 or 12 weeks. Effects on body composition, liver fat, VLDL production rate and the hepatic transcriptome were investigated. [br/] Results: Mice fed the HP diets displayed a lower body weight, developed less adiposity and decreased hepatic lipid accumulation, which could be attributed to a combination of several processes. Next to an increased hepatic VLDL production rate, increased energy utilisation due to enhanced protein catabolic processes, such as transamination, TCA cycle and oxidative phosphorylation was found upon high protein ingestion. [br/] Conclusion: Feeding a HP diet prevented the development of NAFLD by enhancing lipid secretion into VLDL particles and a less efficient use of ingested calories.

International audience; Tripartite motif proteins (TRIM) constitute a large family of proteins containing a RING-Bbox-Coiled Coil motif followed by different C-terminal domains. Involved in ubiquitination, TRIM proteins participate in many cellular processes including antiviral immunity. The TRIM family is ancient and has been greatly diversified in vertebrates and especially in fish. We analyzed the complete sets of trim genes of the large zebrafish genome and of the compact pufferfish genome. Both contain three large multigene subsets--adding the hsl5/trim35-like genes (hltr) to the ftr and the btr that we previously described--all containing a B30.2 domain that evolved under positive selection. These subsets are conserved among teleosts. By contrast, most human trim genes of the other classes have only one or two orthologues in fish. Loss or gain of C-terminal exons generated proteins with different domain organizations; either by the deletion of the ancestral domain or, remarkably, by the acquisition of a new C-terminal domain. Our survey of fish trim genes in fish identifies subsets with different evolutionary dynamics. trims encoding RBCC-B30.2 proteins show the same evolutionary trends in fish and tetrapods: they evolve fast, often under positive selection, and they duplicate to create multigenic families. We could identify new combinations of domains, which epitomize how new trim classes appear by domain insertion or exon shuffling. Notably, we found that a cyclophilin-A domain replaces the B30.2 domain of a zebrafish fintrim gene, as reported in the macaque and owl monkey antiretroviral TRIM5α. Finally, trim genes encoding RBCC-B30.2 proteins are preferentially located in the vicinity of MHC or MHC gene paralogues, which suggests that such trim genes may have been part of the ancestral MHC.