Rapid divergence of mussel populations despite incomplete barriers to dispersal

Striking genetic structure among marine populations at small spatial scales is becoming evident with extensive molecular studies. Such observations suggest isolation at small scales may play an important role in forming patterns of genetic diversity within species. Isolation‐by‐distance, isolation‐by‐environment and historical priority effects are umbrella terms for a suite of processes that underlie genetic structure, but their relative importance at different spatial and temporal scales remains elusive. Here, we use marine lakes in Indonesia to assess genetic structure and assess the relative roles of the processes in shaping genetic differentiation in populations of a bivalve mussel (Brachidontes sp.). Marine lakes are landlocked waterbodies of similar age (6,000–10,000 years), but with heterogeneous environments and varying degrees of connection to the sea. Using a population genomic approach (double‐digest restriction‐site‐associated DNA sequencing), we show strong genetic structuring across populations (range F_ST: 0.07–0.24) and find limited gene flow through admixture plots. At large spatial scales (>1,400 km), a clear isolation‐by‐distance pattern was detected. At smaller spatial scales (<200 km), this pattern is maintained, but accompanied by an association of genetic divergence with degree of connection. We hypothesize that (incomplete) dispersal barriers can cause initial isolation, allowing priority effects to give the numerical advantage necessary to initiate strong genetic structure. Priority effects may be strengthened by local adaptation, which the data may corroborate by showing a high correlation between mussel genotypes and temperature. Our study indicates an often‐neglected role of (evolution‐mediated) priority effects in shaping population divergence.     

TRIM16 controls assembly and degradation of protein aggregates by modulating the p62‐NRF2 axis and autophagy

Sequestration of protein aggregates in inclusion bodies and their subsequent degradation prevents proteostasis imbalance, cytotoxicity, and proteinopathies. The underlying molecular mechanisms controlling the turnover of protein aggregates are mostly uncharacterized. Herein, we show that a TRIM family protein, TRIM16, governs the process of stress‐induced biogenesis and degradation of protein aggregates. TRIM16 facilitates protein aggregate formation by positively regulating the p62‐NRF2 axis. We show that TRIM16 is an integral part of the p62‐KEAP1‐NRF2 complex and utilizes multiple mechanisms for stabilizing NRF2. Under oxidative and proteotoxic stress conditions, TRIM16 activates ubiquitin pathway genes and p62 via NRF2, leading to ubiquitination of misfolded proteins and formation of protein aggregates. We further show that TRIM16 acts as a scaffold protein and, by interacting with p62, ULK1, ATG16L1, and LC3B, facilitates autophagic degradation of protein aggregates. Thus, TRIM16 streamlines the process of stress‐induced aggregate clearance and protects cells against oxidative/proteotoxic stress‐induced toxicity in vitro and in vivo. Taken together, this work identifies a new mechanism of protein aggregate turnover, which could be relevant in protein aggregation‐associated diseases such as neurodegeneration.     

Genetics and genomics of susceptibility and immune response to necrotic enteritis in chicken: a review

Global poultry production is facing many challenges and is currently under pressure due to the presence of several diseases like Necrotic Enteritis (NE). It is estimated that NE-caused global economic losses has increased from 2 billion to 6 billion US$ in 2015 because it is not easy to diagnose and control disease at the earlier stage of occurrence. Additionally, ban on the in-feed antibiotics and some other genetic and non-genetic predisposing factors affect the occurrence of the disease. Though the incidence of the disease can be reduced by minimizing the predisposing factors and through immunization of birds but there is no single remedy to control the disease. Therefore, we suggest that there is need to find out the genetic variants that could help to select the birds resistant to NE. The current review details the pertinent features about the genetic and genomics of susceptibility and immune response of birds to Necrotic Enteritis. We report here the list of candidate gene reported for their involvement with the susceptibility and/or resistance to the disease. However, most of these genes are involved in immune-related functions. For better understanding of the role of Clostridium perfringens and its toxins in the pathogenesis of disease there is need to unveil the association between any specific genetic variation and clinical status of NE. However, the presence of substantial genetic variations among different breeds/strains of chicken shows that it is possible to develop broiler strain with genetic resistant against NE. It would help in the cost-effective and sustainable production of safe broiler meat.     

Abscisic acid and salinity stress induced somaclonal variation and increased histone deacetylase (HDAC) activity in <Emphasis Type="Italic">Ananas comosus</Emphasis> var. MD2

Somaclonal and phenotypic variation caused by genetic and/or epigenetic modifications, are a valuable source of genetic variation to improve desirable polygenetic traits in crops. In this study, we induced somaclonal variation in vitro pineapple (Ananas comosus var. MD2) through hormonal induction, NaCl, and abscisic acid (ABA) supplementation. Our results showed that supplementation of high concentration of 6-benzylaminopurine (4.0 mg/L BAP) alone or combined with indole-butyric acid (IBA) produced the highest percentage of dwarf variants (100%). Murashige and Skoog (MS) media containing 4.0 mg/L BAP plus 2.0 mg/L IBA produced the shortest plantlets (1.9?±?0.1 cm). In comparison, MS media containing 1.0% NaCl induced formation of dwarf plantlets with a mean plantlet height of 1.4?±?0.3 cm, whereas 1.0 mg/L ABA generated plantlets with a mean plantlet height of 1.7?±?0.1 cm. We then analyzed the histone deacetylase (HDAC) enzyme activity for dwarf and non-dwarf plantlets. In general, dwarf plantlets exhibited higher HDAC activity than non-dwarf plantlets. The highest HDAC activity (109, 333.33?±?4.40 ng/min/mg) was recorded for dwarf plantlets grown on media supplemented with 1.0 mg/L ABA. The dwarf variants also underwent phenotypic recovery to normal phenotype within 8 months after transferred to MS basal media. No ploidy alteration was detected in these dwarf plantlets after analyzed by flow cytometry. Taken together, although the generated dwarf plantlets showed higher HDAC activity compared to non-dwarf plantlets, their capability of reverting to non-dwarf phenotype suggested that it might be due to epigenetic modulation.     

Pseudodeficiency of arylsulfatase A: a common genetic polymorphism with possible disease implications

Summary The distribution and frequency of aphidicolin-induced common fragile sites were studied in chromosomes of cultured skin fibroblasts and PHA-stimulated lymphocytes from five normal individuals; 0.2 M aphidicolin was added for the last 26 h of culture. Skin fibroblasts from five fra(X)-positive patients were also studied in the same manner. Fragile sites most frequently found in fibroblasts from normal individuals were 3q26.2, 7q11.23, 16q23, 1p31, 10q11.2, 12q23 and 7q31, whereas those in lymphocytes from the same individuals were 3p14, 16q23, Xp22, 7q32 and 14q24. The distribution of fragile sites in fibroblasts from fra(X)-positive patients was essentially identical with that in normal individuals. The average number of gaps and breaks in 100 metaphases was 36.8 in fibroblasts from normal individuals, 113.8 in those from fra(X)-positive patients, and 279 in lymphocytes from normal individuals. Their rates of chromosome-type breaks and gaps were 7.9%, 29.7% and 54.5%, respectively. Thus, the distribution and frequency of aphidicolin-induced fragile sites were different between skin fibroblasts and lymphocytes, possibly reflecting differences in their DNA replication sequence or gene activity.     

Carnitine long-chain acyltransferase and oxidation of palmitate,palmitoyl coenzyme A and palmitoylcarnitine by pea mitochondria preparations

Palmitoylcarnitine was oxidised by pea mitochondria.l-carnitine was an essential addition for the oxidation of palmitate or palmitoylCoA. When palmitate was sole substrate, ATP and Mg²⁺ were also essential additives for maximum oxidation. Additions of CoA inhibited the oxidation of palmitate. It was shown that CoA was acting as a competitive inhibitor of the carnitine-stimulated O₂ uptake. It is suggested that palmitoylacarnitine and carnitine passed through the mitochondrial barrier with ease but palmitoylCoA and CoA did not. The presence of carnitine long-chain acyl (palmitoyl)transferase (EC 2.3.1.21) in pea-cotyledon mitochondria was shown. This enzyme may play a role in the transport of long-chain acyl groups through membrane barriers.Abbreviation Tris 2-amino-2-(hydroxymethyl)-1,3-propanediol     

Development of Cotton leaf curl virus resistant transgenic cotton using antisense ßC1 gene

Cotton leaf curl virus (CLCuV) is a serious pathogen causing leaf curl disease and affecting the cotton production in major growing areas. The transgenic cotton (Gossypium hirsutum cv. Coker 310) plants were developed by using βC1 gene in antisense orientation gene driven by Cauliflower mosaic virus-35S promoter and nos (nopaline synthase) terminator and mediated by Agrobacterium tumefaciens transformation and somatic embryogenesis system. Molecular confirmation of the transformants was carried out by polymerase chain reaction (PCR) and Southern blot hybridization. The developed transgenic and inoculated plants remained symptomless till their growth period. In conclusion, the plants were observed as resistant to CLCuV.     

Ion mobility mass spectrometry enhances low-abundance species detection in untargeted lipidomics

We describe a simple method for the detection of low intensity lipid signals in complex tissue samples, based on a combination of liquid chromatography/mass spectrometry and ion mobility mass spectrometry. The method relies on visual and software-assisted analysis of overlapped mobilograms (diagrams of mass-to-charge ratio, m/z, vs drift time, DT) and was successfully applied in untargeted lipidomics analyses of mouse brain tissue to detect relatively small variations in a scarce class of phospholipids (N-acyl phosphatidylethanolamines) generated during neural tissue damage, against a background of hundreds of lipid species. Standard analytical tools, including Principal Component Analysis, failed to detect such changes.     

Molecular modeling of Gly80 and Ser80 variants of human group IID phospholipase A2 and their receptor complexes: potential basis for weight loss in chronic obstructive pulmonary disease

Weight loss is a well known systemic manifestation of chronic obstructive pulmonary disease (COPD). A Gly80Ser mutation on human group IID secretory phospholipase A2 (sPLA₂) enhances expression of the cytokines that are responsible for weight loss. In this study, we seek to establish a structural correlation of wild type sPLA₂ and the Gly80Ser mutation with function. sPLA₂ with glycine and serine at the 80th positions and the M-type receptor were modelled. The enzymes were docked to the receptor and molecular dynamics was carried out to 70 ns. Structural analysis revealed the enzymes to comprise three helices (H1–H3), two short helices (SH1 and SH2), and five loops including a calcium binding loop (L1–L5), and to be stabilized by seven disulfide bonds. The overall backbone folds of the two models are very similar, with main chain RMSD of less than 1 Å. The active site within the substrate binding channel shows a catalytic triad of water–His67–Asp112, showing a hydrogen bonded network. Major structural differences between wild type and mutant enzymes were observed locally at the site of the mutation and in their global conformations. These differences include: (1) loop-L3 between H2 and H3, which bears residue Gly80 in the wild type, is in a closed conformation with respect to the channel opening, while in the mutant enzyme it adopts a relatively open conformation; (2) the mutant enzyme is less compact and has higher solvent accessible surface area; and (3) interfacial binding contact surface area is greater, and the quality of interactions with the receptor is better in the mutant enzyme as compared to the wild type. Therefore, the structural differences delineated in this study are potential biophysical factors that could determine the increased potency of the mutant enzyme with macrophage receptor for cytokine secreting function, resulting in exacerbation of cachexia in COPD.