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The objective of the present study was to investigate the effect of dietary phospholipid (PL) level on growth and feed intake of juvenile amberjack ( Seriola dumerili) fed non-fishmeal (non-FM) diet containing alternative protein sources; soybean protein isolate, tuna muscle by-product powder and krill meal. Three non-FM diets were prepared to contain three levels (14, 37 and 54 g kg−1 dry diet) of PL (soybean lecithin acetone insoluble, 886 g kg−1) and growth performance was monitored in a 30-day growth trial by using 2.6 g of fish. The results indicated that final body weight, weight gain and feed intake significantly increased with increasing dietary PL level. At the highest dietary PL level (54 g kg−1 dry diet), the fish consumed 14.8% and 10.2% as much feed as those fish fed diets containing 14 g kg−1 dry diet and 37 g kg−1 dry diet PL, respectively. An increasing tendency with increasing dietary PL level on feed efficiency was observed. In conclusion, the present study demonstrated that dietary PL supplementation could increase feed intake, and improve the growth of juvenile S. dumerili fed non-FM diets. Therefore, purified PL might be a good candidate to stimulate the growth of fish through enhancing the feed intake when they are fed diets containing alternative protein sources. [ABSTRACT FROM AUTHOR]

A feeding experiment was conducted to examine the efficacy of a vitamin C (L-ascorbic acid, AsA) derivative,l-ascorbyl-2-monophosphate Na/Ca (AMP-Na/Ca) by comparing tol-ascorbyl-2-monophosphate-Mg (AMP-Mg) in terms of growth, AsA content in tissues, and hematology in yellowtail Seriola quinqueradiata juvenile (1.10 ± 0.01 g). Furthermore, a stress resistance test for the species fed AMP-Na/Ca was also conducted. In experiment 1, 11 test pellet diets with different levels of AMP-Na/Ca (0, 12, 43, 88, 440 and 881 mg AsA kg−1diet) and AMP-Mg (0, 16, 52, 106, 595 and 1164 mg AsA kg−1 diet) were formulated and fed to the yellowtail three times per day for 50 days. In both the vitamin C sources, the survival rates of the fish fed diets without supplemental AsA were lower than 50% at day 20, and more than 50% mortality occurred in fish that fed the diets containing 12 or 16 mg AsA kg−1 after day 30. However, no significant differences were detected in survival and growth among fish that fed the diets containing more than 43 mg AsA kg−1. Liver and brain AsA concentrations generally increased with increasing dietary AsA level in both sources. In experiment 2, test diets were formulated to contain 43, 88, 440 and 881 mg AsA kg−1 using AMP-Na/Ca, and after 60 days of feeding, yellowtail juveniles were subjected to low salinity and air exposure stress. The fish that received diets with 440 mg AsA kg−1 showed significantly higher tolerance to low salinity stress and higher survival rate in air exposure stress than those of other groups. The present study demonstrated that yellowtail juveniles could utilize AMP-Na/Ca as an AsA source like AMP-Mg, and that supplementation of 43–52 mg AsA kg−1 diet was optimum for normal growth. However, this study showed that dietary inclusion of 440 mg AsA kg−1 would be necessary to improve stress resistance of this species. [ABSTRACT FROM AUTHOR]

The effects of vitamin A palmitate (VAP; 2.7, 27 and 165 mg/100 g diet), β-carotene (βC; 1, 9 and 50 mg/100 g diet) and retinoic acid (RA; 2.8, 28 and 166 mg/100 g diet) on the incidence of deformities in red sea bream (Chrysophrys major) larvae were examined using zein-based micro-bound diets during 15 days. Growth (final body weight, weight gain and total length) and survival rate were affected by the increasing supplementation of these compounds. The abnormalities observed in the larvae included the compression or apparent fusion of the segments in the notochord and mouth deformities. Compression/apparent fusion of the segments was detected mainly in vertebrae of the hemal zone, affecting the total length of larvae. Incidence of these deformities increased with increasing levels of VAP, βC and RA in the diets, but a significantly higher percentage of affected vertebrae was observed in the larvae fed the diets containing RA. The effect of βC was unclear in the present experiment, since only the highest concentration caused significant incidence. The results of this study show that dietary vitamin A may be related to the vertebral deformities in red sea bream larvae. [ABSTRACT FROM AUTHOR]

Recessive gene mutations underlie many developmental disorders and often lead to disabling neurological problems. Here, we report identification of a homozygous c.170G>A (p.Cys57Tyr or C57Y) mutation in the gene coding for protein disulfide isomerase A3 (PDIA3, also known as ERp57), an enzyme that catalyzes formation of disulfide bonds in the endoplasmic reticulum, to be associated with syndromic intellectual disability. Experiments in zebrafish embryos show that PDIA3 C57Y expression is pathogenic and causes developmental defects such as axonal disorganization as well as skeletal abnormalities. Expression of PDIA3 C57Y in the mouse hippocampus results in impaired synaptic plasticity and memory consolidation. Proteomic and functional analyses reveal that PDIA3 C57Y expression leads to dysregulation of cell adhesion and actin cytoskeleton dynamics, associated with altered integrin biogenesis and reduced neuritogenesis. Biochemical studies show that PDIA3 C57Y has decreased catalytic activity and forms disulfide-crosslinked aggregates that abnormally interact with chaperones in the endoplasmic reticulum. Thus, rare disease gene variant can provide insight into how perturbations of neuronal proteostasis can affect the function of the nervous system., (© 2021 MRC Laboratory of Molecular Biology. Published under the terms of the CC BY 4.0 license.)

Objective: Mutations in dysferlin (DYSF), a Ca(2+)-sensitive ferlin family protein important for membrane repair, vesicle trafficking, and T-tubule function, cause Miyoshi myopathy, limb-girdle muscular dystrophy type 2B, and distal myopathy. More than 330 pathogenic DYSF mutations have been identified within exons or near exon-intron junctions. In ~17% of patients who lack normal DYSF, only a single disease-causing mutation has been identified. We studied one family with one known mutant allele to identify both the second underlying genetic defect and potential therapeutic approaches., Methods: We sequenced the full DYSF cDNA and investigated antisense oligonucleotides (AONs) as a tool to modify splicing of the mRNA transcripts in order to process out mutant sequences., Results: We identified a novel pseudoexon between exons 44 and 45, (pseudoexon 44.1, PE44.1), which inserts an additional 177 nucleotides into the mRNA and 59 amino acids within the conserved C2F domain of the DYSF protein. Two unrelated dysferlinopathy patients were also found to carry this mutation. Using AONs targeting PE44.1, we blocked the abnormal splicing event, yielding normal, full-length DYSF mRNA, and increased DYSF protein expression., Interpretation: This is the first report of a deep intronic mutation in DYSF that alters mRNA splicing to include a mutant peptide fragment within a key DYSF domain. We report that AON-mediated exon-skipping restores production of normal, full-length DYSF in patients' cells in vitro, offering hope that this approach will be therapeutic in this genetic context, and providing a foundation for AON therapeutics targeting other pathogenic DYSF alleles.

Schizophrenia is one of the most common and complex neuropsychiatric disorders, which is contributed both by genetic and environmental exposures. Recently, it is shown that NRG1-mediated ErbB4 signalling regulates many important cellular and molecular processes such as cellular growth, differentiation and death, particularly in myelin-producing cells, glia and neurons. Recent association studies have revealed genomic regions of NRG1 and ERBB4, which are significantly associated with risk of developing schizophrenia; however, inconsistencies exist in terms of validation of findings between distinct populations. In this study, we aim to validate the previously identified regions and to discover novel haplotypes of NRG1 and ERBB4 using logistic regression models and Haploview analyses in three independent datasets from GWAS conducted on European subjects, namely, CATIE, GAIN and nonGAIN. We identified a significant 6-kb block in ERBB4 between chromosome locations 212,156,823 and 212,162,848 in CATIE and GAIN datasets (p = 0.0206 and 0.0095, respectively). In NRG1, a significant 25-kb block, between 32,291,552 and 32,317,192, was associated with risk of schizophrenia in all CATIE, GAIN, and nonGAIN datasets (p = 0.0005, 0.0589, and 0.0143, respectively). Fine mapping and FastSNP analysis of genetic variation located within significantly associated regions proved the presence of binding sites for several transcription factors such as SRY, SOX5, CEPB, and ETS1. In this study, we have discovered and validated haplotypes of ERBB4 and NRG1 in three independent European populations. These findings suggest that these haplotypes play an important role in the development of schizophrenia by affecting transcription factor binding affinity.