Characterization of miR-206 Promoter and Its Association with Birthweight in Chicken

miRNAs have been widely investigated in terms of cell proliferation and differentiation. However, little is known about their effects on bird growth. Here we characterized the promoter of miR-206 in chicken and found that the preferable promoter was located in 1200 bp upstream of pri-miR-206. In this region, many key transcription factors, including MyoD, c-Myb, CEBPα/β, AP-4, RAP1, Brn2, GATA-1/2/3, E47, Sn, upstream stimulatory factor (USF) and CdxA, were predicted to bind and interact with miR-206 promoter. Overexpression of MyoD sharply increased miR-206 expression in both fibroblast and myoblast cells, and also the regulation in the myoblast cells was much stronger, indicating that miR-206 was regulated by MyoD combined with other muscle specific transcriptional factors. Aiming to further investigate the relationship between miR-206 mutation and transcriptional expression, total of 23 SNPs were identified in the two distinct bird lines by sequencing. Interestingly, the motif bound by MyoD was individually destroyed by G-to-C mutation located at 419 bp upstream of miR-206 precursor. Co-transfecting MyoD and miR-206 promoter in DF-1 cells, the luciferase activity of promoter containing homozygous GG types was significantly higher than CC ones (p < 0.05). Thus, this mutation caused low expression of miR-206. Consistently, eight variants including G-419C mutation exhibited a great effect on birthweight through maker-trait association analysis in F2 population (p < 0.05). Additionally, the regulation of miR-206 on embryo muscle mass mainly by increasing MyoG and muscle creatine kinase (MCK) expression (p < 0.05) with little change in MyoD, TMEM8C and myosin heavy chain (MHC). In conclusion, our findings provide a novel mutation destroying the promoter activity of miR-206 in birds and shed new light to understand the regulation mechanism of miR-206 on the embryonic muscle growth

A short insertion mutation disrupts genesis of miR-16 and causes increased body weight in domesticated chicken

Body weight is one of the most important quantitative traits with high heritability in chicken. We previously mapped a quantitative trait locus (QTL) for body weight by genome-wide association study (GWAS) in an F2 chicken resource population. To identify the causal mutations linked to this QTL, expression profiles were determined on livers of high-weight and low-weight chicken lines by microarray. Combining the expression pattern with SNP effects by GWAS, miR-16 was identified as the most likely potential candidate with a 3.8-fold decrease in high-weight lines. Re-sequencing revealed that a 54-bp insertion mutation in the upstream region of miR-15a-16 displayed high allele frequencies in high-weight commercial broiler line. This mutation resulted in lower miR-16 expression by introducing three novel splicing sites instead of the missing 5′ terminal splicing of mature miR-16. Elevating miR-16 significantly inhibited DF-1 chicken embryo cell proliferation, consistent with a role in suppression of cellular growth. The 54-bp insertion was significantly associated with increased body weight, bone size and muscle mass. Also, the insertion mutation tended towards fixation in commercial broilers (Fst > 0.4). Our findings revealed a novel causative mutation for body weight regulation that aids our basic understanding of growth regulation in birds.This article is published as Jia, Xinzheng, Huiran Lin, Qinghua Nie, Xiquan Zhang, and Susan J. Lamont. "A short insertion mutation disrupts genesis of miR-16 and causes increased body weight in domesticated chicken." Scientific Reports 6 (2016): 36433. DOI: 10.1038/srep36433. Posted with permission.</p

Pd/ZnO catalysts with different origins for high chemoselectivity in acetylene semi-hydrogenation

The heterogeneity of active sites is the main obstacle for selectivity control in heterogeneous catalysis. Single atom catalysts (SACS) with homogeneous isolated active sites are highly desired in chemoselective transformations. In this work, a Pd-1/ZnO catalyst with single-atom dispersion of Pd active sites was achieved by decreasing the Pd loading and reducing the sample at a relatively low temperature. The Pd-1/ZnO SAC exhibited excellent catalytic performance in the chemoselective hydrogenation of acetylene with comparable chemoselectivity to that of PdZn intermetallic catalysts and a greatly enhanced utilization of Pd metal. Such unusual behaviors of the Pd-1/ZnO SAC in acetylene semi-hydrogenation were ascribed to the high-valent single Pd active sites, which could promote electrostatic interactions with acetylene but restrain undesired ethylene hydrogenation via the spatial restrictions of o-chemical bonding toward ethylene. (C) 2016, Dalian Institute of Chemical Physics, Chinese Academy of Sciences. Published by Elsevier B.V. All rights reserved

Opposite effective connectivity in the posterior cingulate and medial prefrontal cortex between first-episode schizophrenic patients with suicide risk and healthy controls.

OBJECTIVE: The schizophrenic patients with high suicide risk are characterized by depression, better cognitive function, and prominent positive symptoms. However, the neurobiological basis of suicide attempts in schizophrenia is not clear. The suicide in schizophrenia is implicated in the defects in emotional process and decision-making, which are associated with prefrontal-cingulate circuit. In order to explore the possible neurobiological basis of suicide in schizophrenia, we investigated the correlation of prefrontal-cingulate circuit with suicide risk in schizophrenia via dynamic casual modelling. METHOD: Participants were 33 first-episode schizophrenic patients comprising of a high suicide risk group (N = 14) and a low suicide risk group (N = 19). A comparison group of healthy controls (N = 15) were matched for age, gender and education. N-back tasking functional magnetic resonance imaging data was collected. RESULTS: Compared with healthy controls group, the two patients groups showed decreased task-related suppression during 2-back task state versus baseline state in the left posterior cingulate and medial prefrontal cortex; the hyper-connectivity from the left posterior cingulate cortex to the left medial prefrontal cortex existed in both schizophrenic patients groups, but hypo-connectivity in the opposite direction only existed in the schizophrenic patients group with high suicide risk. CONCLUSIONS: The hyper-connectivity from the left posterior cingulate cortex to the left medial prefrontal cortex may suggest that the abnormal effective connectivity was associated with risk for schizophrenia. The hypo-connectivity in the opposite direction may represent a possible correlate of increased vulnerability to suicide attempt

PdZn Intermetallic Nanostructure with Pd–Zn–Pd Ensembles for Highly Active and Chemoselective Semi-Hydrogenation of Acetylene

Intermetallic alloying of one active metal to another inert metal provides not only the improved dispersion of active centers but also a unique and homogeneous ensemble of active sites, thus offering new opportunities in a variety of reactions. Herein, we report that PdZn intermetallic nanostructure with Pd–Zn–Pd ensembles are both highly active and selective for the semihydrogenation of acetylene to ethylene, which is usually inaccessible due to the sequential hydrogenation to ethane. Microcalorimetric measurements and density functional theory calculations demonstrate that the appropriate spatial arrangement of Pd sites in the Pd–Zn–Pd ensembles of the PdZn alloy leads to the moderate σ-bonding mode for acetylene with two neighboring Pd sites while the weak π-bonding pattern of ethylene adsorption on the single Pd site, which facilitates the chemisorption toward acetylene and promotes the desorption of ethylene from the catalyst surface. As a result, it leads to the kinetic favor of the selective conversion of acetylene to ethylene

Five hypothesized dynamic casual models during 2-back task.

<p>Each model includes the left medial prefrontal cortex (MPFC) and the ipsilateral posterior cingulate cortex (PCC), in which the arrows indicate extrinsic stimulation and functional connections direction. M1, M2 and M3 comprised bi-directional connections with respectively driving input into PCC or MPFC or both of the regions. M4 only contained unidirectional connection from the PCC to MPFC with driving input into PCC and M5 was completely opposite to M4. M1, M4 and M2 were identified as the optimal models in HSR, LSR and HC respectively. HSR: schizophrenic patients with high suicide risk; LSR: schizophrenic patients with low suicide risk; HC: healthy controls.</p

Regions with significant activations at rest state compared with 2-back task (<i>p</i><0.05, FWE corrected).

<p>Regions with significant activations at rest state compared with 2-back task (<i>p</i><0.05, FWE corrected).</p

Regions with significant activations at rest state among three groups compared with 2-back task.

<p>From A to D (upper part), brain areas are left medial prefrontal cortex (MPFC), left posterior cingulate cortex (PCC), left middle frontal gyrus and right precentral gyrus (<i>p</i><0.005, cluster >20). The signal changes in MPFC and PCC in the three groups are shown below (a and b). Error bars indicated 2 standard errors (SE), *<i>p<</i>0.05.</p

The demographic and clinical characteristics for high suicide risk group (HSR), low suicide risk group (LSR) and healthy controls group (HC).

<p>Data reflect mean (SD) unless otherwise stated. “–” reflect not applicable; “*” means significant statistical difference (statistical threshold <i>p</i><0.05). WAIS-I = Information subscale of the Wechsler Adult Intelligence Scale-Chinese Revised; WAIS-DS = Digit Symbol subscale of the Wechsler Adult Intelligence Scale-Chinese Revised; SAPS = Scale for the Assessment of Positive Symptoms; SANS = Scale for the Assessment of Negative Symptoms; SSRS = Schizophrenia Suicide Risk Scale; CPZ = Chlorpromazine. The proportion correct responses and response time(s) for correct responses were the performance during 2-back task.</p