First Insight into Exploration and Cognition in Wild Caught and Domesticated Sea Bass (Dicentrarchus labrax) in a Maze

European sea bass aquaculture is so recent that very little is known on the effects of the early steps of its domestication. Behavioural parameters are sensitive indicators of the domestication process since they are generally impacted as soon as the first generation. The present work compared wild-caught and domesticated sea bass juvenile swimming activity, exploration and ability to learn to discriminate between two 2-D objects associated to a simple spatial task that enabled the tested individual to visually interact with an unfamiliar congener (the reward) located behind a transparent wall at the end of one of the two arms of a maze. Ten fish from each origin were individually tested 3 times in a row during 3 days (9 trials in total). Fish were placed in a start box closed by a transparent wall located in front of two 2-D objects. Fish were filmed during 10 min after the removal of the start box wall. Different swimming variables including angular velocity, total distance travelled and velocity mean, were analyzed from videos as well as the time spent in each of 6 virtual zones including the reward zone near the congener (Cong) and the zone opposite to the reward zone (OpCong). Two learning criteria were chosen: the number of successful turns and time to reach Cong. Behavioural differences were found between domesticated and wild fish. Angular velocity was higher in wild fish while the distance travelled and the velocity mean were higher in domesticated ones. Wild and domesticated fish spent most of the time in Cong and in OpCong. No differences were seen in learning ability between wild and domesticated fish. However, our findings for learning require confirmation by further studies with larger numbers of learning sessions and experiments designed to minimise stress. This study therefore demonstrated an impact of domestication on swimming behaviour but not on spatial learning.     

Expression of rod-derived cone viability factor: dual role of CRX in regulating promoter activity and cell-type specificity

Background

RdCVF and RdCVF2, encoded by the nucleoredoxin-like genes NXNL1 and NXNL2, are trophic factors with therapeutic potential that are involved in cone photoreceptor survival. Studying how their expression is regulated in the retina has implications for understanding both their activity and the mechanisms determining cell-type specificity within the retina.

Methodology/Principal Findings

In order to define and characterize their promoters, a series of luciferase/GFP reporter constructs that contain various fragments of the 5′-upstream region of each gene, both murine and human, were tested in photoreceptor-like and non-photoreceptor cell lines and also in a biologically more relevant mouse retinal explant system. For NXNL1, 5′-deletion analysis identified the human −205/+57 bp and murine −351/+51 bp regions as having promoter activity. Moreover, in the retinal explants these constructs drove expression specifically to photoreceptor cells. For NXNL2, the human −393/+27 bp and murine −195/+70 bp regions were found to be sufficient for promoter activity. However, despite the fact that endogenous NXNL2 expression is photoreceptor-specific within the retina, neither of these DNA sequences nor larger upstream regions demonstrated photoreceptor-specific expression. Further analysis showed that a 79 bp NXNL2 positive regulatory sequence (−393 to 315 bp) combined with a 134 bp inactive minimal NXNL1 promoter fragment (−77 to +57 bp) was able to drive photoreceptor-specific expression, suggesting that the minimal NXNL1 fragment contains latent elements that encode cell-type specificity. Finally, based on bioinformatic analysis that suggested the importance of a CRX binding site within the minimal NXNL1 fragment, we found by mutation analysis that, depending on the context, the CRX site can play a dual role.

Conclusions/Significance

The regulation of the Nucleoredoxin-like genes involves a CRX responsive element that can act as both as a positive regulator of promoter activity and as a modulator of cell-type specificity.     

Characterization of Halanaerobaculum tunisiense gen. nov., sp. nov., a new halophilic fermentative, strictly anaerobic bacterium isolated from a hypersaline lake in Tunisia

A new halophilic anaerobe was isolated from the hypersaline surface sediments of El-Djerid Chott, Tunisia. The isolate, designated as strain 6SANG, grew at NaCl concentrations ranging from 14 to 30%, with an optimum at 20–22%. Strain 6SANG was a non-spore-forming, non-motile, rod-shaped bacterium, appearing singly, in pairs, or occasionally as long chains (0.7–1 × 4–13 μm) and showed a Gram-negative-like cell wall pattern. It grew optimally at pH values between 7.2 and 7.4, but had a very broad pH range for growth (5.9–8.4). Optimum temperature for growth was 42°C (range 30–50°C). Strain 6SANG required yeast extract for growth on sugars. Glucose, sucrose, galactose, mannose, maltose, cellobiose, pyruvate, and starch were fermented. The end products from glucose fermentation were acetate, butyrate, lactate, H₂, and CO₂. The G + C ratio of the DNA was 34.3 mol%. Strain 6SANG exhibited 16S rRNA gene sequence similarity values of 91–92% with members of the genus Halobacteroides, H. halobius being its closest phylogenetic relative. Based on phenotypic and phylogenetic characteristics, we propose that this bacterium be classified as a novel species of a novel genus, Halanaerobaculum tunisiense gen. nov., sp. nov. The type strain is 6SANG^T (=DSM 19997^T = JCM 15060^T).     

Contribution of NZB autoimmunity 2 to Y-linked autoimmune acceleration-induced monocytosis in association with murine systemic lupus

The accelerated development of systemic lupus erythematosus (SLE) in BXSB male mice is associated with the presence of the Y-linked autoimmune acceleration (Yaa) mutation, which induces an age-dependent monocytosis. Using a cohort of C57BL/6 (B6) x (NZB x B6)F1 backcross male mice bearing the Yaa mutation, we defined the pathogenic role and genetic basis for Yaa-associated monocytosis. We observed a remarkable correlation of monocytosis with autoantibody production and subsequent development of lethal lupus nephritis, indicating that monocytosis is an additional useful indicator for severe SLE. In addition, we identified an NZB-derived locus on chromosome 1 predisposing to the development of monocytosis, which peaked at Fcgr2b encoding FcgammaRIIB and directly overlapped with the previously identified NZB autoimmunity 2 (Nba2) locus. The contribution of Nba2 to monocytosis was confirmed by the analysis of Yaa-bearing B6 mice congenic for the NZB-Nba2 locus. Finally, we observed a very low-level expression of FcgammaRIIB on macrophages bearing the NZB-type Fcgr2b allele, compared with those bearing the B6-type allele, and the development of monocytosis in FcgammaRIIB haploinsufficient B6 mice carrying the Yaa mutation. These data suggest that the Nba2 locus may play a supplementary role in the pathogenesis of SLE by promoting the development of monocytosis and the activation of effector cells bearing stimulatory FcgammaR, in addition to its implication in the dysregulated activation of autoreactive B cells.     

The inhibiting Fc receptor for IgG, FcγRIIB, is a modifier of autoimmune susceptibility

FcγRIIB-deficient mice generated in 129 background (FcγRIIB(129)(-/-)) if back-crossed into C57BL/6 background exhibit a hyperactive phenotype and develop lethal lupus. Both in mice and humans, the Fcγr2b gene is located within a genomic interval on chromosome 1 associated with lupus susceptibility. In mice, the 129-derived haplotype of this interval, named Sle16, causes loss of self-tolerance in the context of the B6 genome, hampering the analysis of the specific contribution of FcγRIIB deficiency to the development of lupus in FcγRIIB(129)(-/-) mice. Moreover, in humans genetic linkage studies revealed contradictory results regarding the association of "loss of function" mutations in the Fcγr2b gene and susceptibility to systemic lupus erythematosis. In this study, we demonstrate that FcγRIIB(-/-) mice generated by gene targeting in B6-derived ES cells (FcγRIIB(B6)(-/-)), lacking the 129-derived flanking Sle16 region, exhibit a hyperactive phenotype but fail to develop lupus indicating that in FcγRIIB(129)(-/-) mice, not FcγRIIB deficiency but epistatic interactions between the C57BL/6 genome and the 129-derived Fcγr2b flanking region cause loss of tolerance. The contribution to the development of autoimmune disease by the resulting autoreactive B cells is amplified by the absence of FcγRIIB, culminating in lethal lupus. In the presence of the Yaa lupus-susceptibility locus, FcγRIIB(B6)(-/-) mice do develop lethal lupus, confirming that FcγRIIB deficiency only amplifies spontaneous autoimmunity determined by other loci.     

Integrative epigenomic mapping defines four main chromatin states in Arabidopsis

Post-translational modification of histones and DNA methylation are important components of chromatin-level control of genome activity in eukaryotes. However, principles governing the combinatorial association of chromatin marks along the genome remain poorly understood. Here, we have generated epigenomic maps for eight histone modifications (H3K4me2 and 3, H3K27me1 and 2, H3K36me3, H3K56ac, H4K20me1 and H2Bub) in the model plant Arabidopsis and we have combined these maps with others, produced under identical conditions, for H3K9me2, H3K9me3, H3K27me3 and DNA methylation. Integrative analysis indicates that these 12 chromatin marks, which collectively cover ～90% of the genome, are present at any given position in a very limited number of combinations. Moreover, we show that the distribution of the 12 marks along the genomic sequence defines four main chromatin states, which preferentially index active genes, repressed genes, silent repeat elements and intergenic regions. Given the compact nature of the Arabidopsis genome, these four indexing states typically translate into short chromatin domains interspersed with each other. This first combinatorial view of the Arabidopsis epigenome points to simple principles of organization as in metazoans and provides a framework for further studies of chromatin-based regulatory mechanisms in plants.