The complete mitochondrial genome of the wild silkworm moth, Actias selene

The complete mitochondrial genome (mitogenome) of Actias selene (Lepidoptera: Saturniidae) was determined to be 15,236 bp, including 13 protein-coding genes (PCGs), two rRNA genes, 22 tRNA genes and a control region. The arrangement of 13 PCGs was similar to that of other sequenced lepidopterans. The AT skew of the mitogenome of A. selene was slightly negative, indicating a higher number of T compared to A nucleotides. The nucleotide composition of the mitogenome of A. selene was also biased toward A+T nucleotides (78.91%). All PCGs were initiated by ATN codons, except for the gene encoding cytochrome c oxidase subunit 1 (cox1), which may be initiated by the TTAG, as observed in other lepidopterans. Three genes, including cox1, cox2, and nad5, had incomplete stop codons consisting of just a T. With an exception for trnS1(AGN), all the other tRNA genes displayed a typical clover-leaf structure of mitochondrial tRNA. The A+T-rich region of the mitogenome of A. selene was 339 bp in length, and contains several features common to the Lepidopteras, including non-repetitive sequences, a conserved structure combining the motif ATAGA and an 18-bp poly-T stretch and a poly-A element upstream of trnM gene. Phylogenetic analysis showed that A. selene was close to Saturniidae.     

Neurturin-GFRalpha2 signaling controls liver bud migration along the ductus venosus in the chick embryo

During chick liver development, the liver bud arises from the foregut, invaginates into the septum transversum, and elongates along and envelops the ductus venosus. However, the mechanism of liver bud migration is only poorly understood. Here, we demonstrate that a GDNF family ligand involved in neuronal outgrowth and migration, neurturin (NRTN), and its receptor, GFRalpha2, are essential for liver bud migration. In the chick embryo, we found that GFRalpha2 was expressed in the liver bud and that NRTN was expressed in the endothelial cells of the ductus venosus. Inhibition of GFRalpha2 signaling suppressed liver bud elongation along the ductus venous without affecting cell proliferation and apoptosis. Moreover, ectopic expression of NRTN perturbed the directional migration along the ductus venosus, leading to splitting or ectopic branching of the liver. We showed that liver buds selectively migrated toward an NRTN-soaked bead in vitro. These data represent a new model for liver bud migration: NRTN secreted from endothelial cells functions as a chemoattractant to direct the migration of the GFRalpha2-expressing liver bud in early liver development.     

Complete mitochondrial genome of a forensically important muscid, Hydrotaea chalcogaster (Diptera: Muscidae), with notes on its phylogenetic position

Muscidae are a dipteran family which is important for forensic investigations. However, it has received limited attention in forensic entomological experiments as a reason of identification issues. It is hard to identify specimens by morphological methods, especially in developmental stages. Therefore, complete mitochondrial genome sequences can be important tool in forensic entomology for identifying species. In this study we sequenced and analyzed the first complete mitochondrial genome from a forensically important Muscidae species Hydrotaea (=Ophyra) chalcogaster by next-generation sequencing. The mitochondrial genome of the sequenced species is circular molecules of 17,076?bp which have the typical mitochondrial genome complement of 13 protein-coding genes, 22 tRNAs, two ribosomal RNA genes and a control region. Rearrangements of gene positions are identical with the ancestral insect genome. Furthermore, phylogenetic relationships of the family Muscidae were evaluated in regard to mitochondrial protein coding genes. The inferred trees indicate that the Muscidae is a paraphyletic family. These data provide additional information for molecular identification of muscid species.     

Astrocytic metabolic and inflammatory changes as a function of age

This study examines age‐dependent metabolic‐inflammatory axis in primary astrocytes isolated from brain cortices of 7‐, 13‐, and 18‐month‐old Sprague–Dawley male rats. Astrocytes showed an age‐dependent increase in mitochondrial oxidative metabolism respiring on glucose and/or pyruvate substrates; this increase in mitochondrial oxidative metabolism was accompanied by increases in COX3/18SrDNA values, thus suggesting an enhanced mitochondrial biogenesis. Enhanced mitochondrial respiration in astrocytes limits the substrate supply from astrocytes to neurons; this may be viewed as an adaptive mechanism to altered cellular inflammatory–redox environment with age. These metabolic changes were associated with an age‐dependent increase in hydrogen peroxide generation (largely ascribed to an enhanced expression of NOX2) and NFκB signaling in the cytosol as well as its translocation to the nucleus. Astrocytes also displayed augmented responses with age to inflammatory cytokines, IL‐1β, and TNFα. Activation of NFκB signaling resulted in increased expression of nitric oxide synthase 2 (inducible nitric oxide synthase), leading to elevated nitric oxide production. IL‐1β and TNFα treatment stimulated mitochondrial oxidative metabolism and mitochondrial biogenesis in astrocytes. It may be surmised that increased mitochondrial aerobic metabolism and inflammatory responses are interconnected and support the functionality switch of astrocytes, from neurotrophic to neurotoxic with age.     

Determination of total and active immobilized enzyme distribution in porous solid supports

The total and active immobilized enzyme (IME) distributions in porous supports are studied both theoretically and experimentally. In order to determine experimentally the enzyme distribution profiles within a single particle, we construct a diffusion cell containing controlled-pore glass particles such that the cell would mimic a large pellet support. Our purpose is to study the interplay between the diffusion process within the interparticle void space and immobilization process in the controlled-pore glass particles onto the evolution of the (total and active) enzyme distributions. A mathematical model is developed to describe the interaction of various processes within the diffusion cell. The immobilized enzymes are determined for a system of trypsin and controlled-pore glass particles. The total amount of enzymes are determined by the amino acid analysis, and the active fraction is obtained by an active-site titration. The experimentally measured total IME profiles compare very well with that predicted by the model. The determined active enzyme profile is found to be nonuniform one, and it represents about 40% of the total enzyme immobilized in the support particles.     

Hepatocellular protection by nitric oxide or nitrite in ischemia and reperfusion injury

Ischemia and reperfusion (I/R)-induced liver injury occurs in several pathophysiological disorders including hemorrhagic shock and burn as well as resectional and transplantation surgery. One of the earliest events associated with reperfusion of ischemic liver is endothelial dysfunction characterized by the decreased production of endothelial cell-derived nitric oxide (NO). This rapid post-ischemic decrease in NO bioavailability appears to be due to decreased synthesis of NO, enhanced inactivation of NO by the overproduction of superoxide or both. This review presents the most current evidence supporting the concept that decreased bioavailability of NO concomitant with enhanced production of reactive oxygen species initiates hepatocellular injury and that endogenous NO or exogenous NO produced from nitrite play important roles in limiting post-ischemic tissue injury.     

Mitochondrial Oxidative Phosphorylation Regulates the Fate Decision between Pathogenic Th17 and Regulatory T Cells

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Multilocus phylogeography of the Patagonian lizard complex Liolaemus kriegi (Iguania: Liolaemini)

This study presents a detailed phylogeographical analysis of one of the most conspicuous groups of lizards in northwestern Patagonia, the Liolaemus kriegi complex. This region is geographically very complex as a result of Andean orogeny and subsequent volcanism coupled with a long history of glaciations and climatic changes. For 247 individuals we sequenced one mitochondrial gene (cytochrome b) and for a subset we sequenced another mitochondrial gene [12S ribosomal RNA (12S)] and two nuclear fragments [kinesin family member 24 (KIF24) and BA3 ribosomal RNA (BA3)]. We obtained gene trees and mitochondrial and nuclear haploytpe networks, and estimated genetic distances between the main lineages and basic molecular diversity indices. We also performed spatial analysis of molecular variance (SAMOVA) and Bayesian Skyline Plot (BSP) analyses, and concordant patterns from different lines of evidence permitted delimitation of seven lineages: two described species, Liolaemus buergeri and Liolaemus tregenzai; four candidate species, Liolaemus sp. A, Liolaemus sp. B, Liolaemus sp. C, and Liolaemus sp. D; and one lineage that includes all individuals from the geographical range of Liolaemus ceii and L. kriegi, referred to as L. kriegi + L. ceii. We discuss the evolutionary processes that may contribute to the origin of these lineages and their taxonomic and conservation implications. © 2014 The Linnean Society of London, Biological Journal of the Linnean Society, 2014, 113 , 256–269.     

Cardiac mitochondrial ATP-sensitive potassium channel is activated by nitric oxide in vitro

Previous observations on the activation of the mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) by nitric oxide (NO) in myocardial preconditioning were based on indirect evidence. In this study, we have investigated the direct effect of NO on the rat cardiac mitoK(ATP) after reconstitution of the inner mitochondrial membranes into lipid bilayers. We found that the mitoK(ATP) was activated by exogenous NO donor S-nitroso-N-acetyl penicillamine or PAPA NONOate. This activation was inhibited by mitoK(ATP) blockers 5-hydroxydecanoate or glibenclamide. Our observations confirm that NO can directly activate the cardiac mitoK(ATP), which may underlie its contribution to myocardial preconditioning.