Ultra‐Conserved Elements and morphology reciprocally illuminate conflicting phylogenetic hypotheses in Chalcididae (Hymenoptera,Chalcidoidea)

Recent technical advances combined with novel computational approaches have promised the acceleration of our understanding of the tree of life. However, when it comes to hyperdiverse and poorly known groups of invertebrates, studies are still scarce. As published phylogenies will be rarely challenged by future taxonomists, careful attention must be paid to potential analytical bias. We present the first molecular phylogenetic hypothesis for the family Chalcididae, a group of parasitoid wasps, with a representative sampling (144 ingroups and seven outgroups) that covers all described subfamilies and tribes, and 82% of the known genera. Analyses of 538 Ultra‐Conserved Elements (UCEs) with supermatrix (RAx ML and IQTREE) and gene tree reconciliation approaches (ASTRAL, ASTRID) resulted in highly supported topologies in overall agreement with morphology but reveal conflicting topologies for some of the deepest nodes. To resolve these conflicts, we explored the phylogenetic tree space with clustering and gene genealogy interrogation methods, analyzed marker and taxon properties that could bias inferences and performed a thorough morphological analysis (130 characters encoded for 40 taxa representative of the diversity). This joint analysis reveals that UCEs enable attainment of resolution between ancestry and convergent/divergent evolution when morphology is not informative enough, but also shows that a systematic exploration of bias with different analytical methods and a careful analysis of morphological features is required to prevent publication of artifactual results. We highlight a GC content bias for maximum‐likelihood approaches, an artifactual mid‐point rooting of the ASTRAL tree and a deleterious effect of high percentage of missing data (>85% missing UCEs) on gene tree reconciliation methods. Based on the results we propose a new classification of the family into eight subfamilies and ten tribes that lay the foundation for future studies on the evolutionary history of Chalcididae.     

Characterization of the cell death induced by cadmium in HaCaT and C6 cell lines

Cell death resulting from cadmium (Cd) intoxication has been confirmed to induce both necrosis and apoptosis. The ratio between both types of cell death is dose- and cell-type-dependent. This study used the human keratinocytes HaCaT expressing a mutated p53 and the rat glial cells C6 expressing a wild p53 as models to characterize Cd-induced apoptosis, using sub-lethal and lethal doses. At these concentrations, features of apoptosis were observed 24 h after C6 cell treatment: apoptotic DNA fragmentation and caspase-9 activation, whereas Cd did not induce caspase-3. In HaCaT, Cd did not induce apoptotic DNA fragmentation or caspase-9 and -3 activation. The results also showed that the inhibition of p53 led to a resistance of the C6 cells to 20 µm Cd, decreased the apoptosis and increased the metallothioneins in these cells. p53 restoration increased the sensitivity of HaCaT cells to Cd but did not affect the MT expression. The results suggest that Cd induced apoptosis in C6 cells but a non-apoptotic cellular death in HaCaT cells.     

Acute Hypoxemia Does Not Increase the Oxidative Stress in Resting and Contracting Muscle in Humans

In healthy humans sustaining static handgrip at 60% of maximal voluntary contraction (MVC) until exhaustion, we measured the venous blood concentration of reduced ascorbic acid (RAA) and thiobarbituric acid reactive substances (TBARS), respectively, used as markers of the post-exercise oxidative stress and lipid peroxidation. Measurements were conducted in normoxemia, then during a 30-min period of hypoxemia (PaO 2 =56 mmHg) produced by inhalation of an hypoxic gas mixture. Compared to normoxemia, hypoxemia did not significantly modify the resting concentrations of TBARS and RAA, and did not affect the consumption of ascorbic acid after 60% MVC but suppressed the post-exercise TBARS increase. We conclude that acute hypoxemia does not modify the production of oxygen free radicals after strenuous static efforts and even seems to attenuate the lipid peroxidation.     

The genera in the second catalogue (1833–1836) of?Dejean’s Coleoptera collection

All genus-group names listed in the second edition of the catalogue (1833-1836) of Dejean’s beetle collection are recorded. For each new genus-group name the originally included available species are listed and for generic names with at least one available species, the type species and the current status are given. Names available prior to the publication of Dejean’s second catalogue (1833-1836) are listed in an appendix.The following new synonymies are proposed: Cyclonotum Dejean, 1833 (= Dactylosternum Wollaston, 1854) [Hydrophilidae], Hyporhiza Dejean, 1833 (= Rhinaspis Perty, 1830) [Scarabaeidae], Aethales Dejean, 1834 (= Epitragus Latreille, 1802) [Tenebrionidae], Arctylus Dejean, 1834 (= Praocis Eschscholtz, 1829) [Tenebrionidae], Euphron Dejean, 1834 (= Derosphaerus Thomson, 1858) [Tenebrionidae], Hipomelus Dejean, 1834 (= Trachynotus Latreille, 1828) [Tenebrionidae], Pezodontus Dejean, 1834 (= Odontopezus Alluaud, 1889) [Tenebrionidae], Zygocera Dejean, 1835 (= Disternopsis Breuning, 1939) [Cerambycidae], and Physonota Chevrolat, 1836 (= Anacassis Spaeth, 1913) [Chrysomelidae]. Heterogaster pilicornis Dejean, 1835 [Cerambycidae] and Labidomera trimaculata Chevrolat, 1836 [Chrysomelidae] are placed for the first time in synonymy with Anisogaster flavicans Deyrolle, 1862 and Chrysomela clivicollis Kirby, 1837 respectively. Type species of the following genus-group taxa are proposed: Sphaeromorphus Dejean, 1833 (Sphaeromorphus humeralis Erichson, 1843) [Scarabaeidae], Adelphus Dejean, 1834 (Helops marginatus Fabricius, 1792) [Tenebrionidae], Cyrtoderes Dejean, 1834 (Tenebrio cristatus DeGeer, 1778) [Tenebrionidae], Selenepistoma Dejean, 1834 (Opatrum acutum Wiedemann, 1823) [Tenebrionidae], Charactus Dejean, 1833 (Lycus limbatus Fabricius, 1801) [Lycidae], Corynomalus Chevrolat, 1836 (Eumorphus limbatus Olivier, 1808) [Endomychidae], Hebecerus Dejean, 1835 (Acanthocinus marginicollis Boisduval, 1835) [Cerambycidae], Pterostenus Dejean, 1835 (Cerambyx abbreviatus Fabricius, 1801) [Cerambycidae], Psalicerus Dejean, 1833 (Lucanus femoratus Fabricius, 1775) [Lucanidae], and Pygolampis Dejean, 1833 (Lampyris glauca Olivier, 1790) [Lampyridae]. A new name, Neoeutrapela Bousquet and Bouchard [Tenebrionidae], is proposed for Eutrapela Dejean, 1834 (junior homonym of Eutrapela Hübner, 1809).The following generic names, made available in Dejean’s catalogue, were found to be older than currently accepted valid names: Catoxantha Dejean, 1833 over Catoxantha Solier, 1833 [Buprestidae], Pristiptera Dejean, 1833 over Pelecopselaphus Solier, 1833 [Buprestidae], Charactus Dejean, 1833 over Calopteron Laporte, 1836 [Lycidae], Cyclonotum Dejean, 1833 over Dactylosternum Wollaston, 1854 [Hydrophilidae], Ancylonycha Dejean, 1833 over Holotrichia Hope, 1837 [Scarabaeidae], Aulacium Dejean, 1833 over Mentophilus Laporte, 1840 [Scarabaeidae], Sciuropus Dejean, 1833 over Ancistrosoma Curtis, 1835 [Scarabaeidae], Sphaeromorphus Dejean, 1833 over Ceratocanthus White, 1842 [Scarabaeidae], Psalicerus Dejean, 1833 over Leptinopterus Hope, 1838 [Lucanidae], Adelphus Dejean, 1834 over Praeugena Laporte, 1840 [Tenebrionidae], Amatodes Dejean, 1834 over Oncosoma Westwood, 1843 [Tenebrionidae], Cyrtoderes Dejean, 1834 over Phligra Laporte, 1840 [Tenebrionidae], Euphron Dejean, 1834 over Derosphaerus Thomson, 1858 [Tenebrionidae], Pezodontus Dejean, 1834 over Odontopezus Alluaud, 1889 [Tenebrionidae], Anoplosthaeta Dejean, 1835 over Prosopocera Blanchard, 1845 [Cerambycidae], Closteromerus Dejean, 1835 over Hylomela Gahan, 1904 [Cerambycidae], Hebecerus Dejean, 1835 over Ancita Thomson, 1864 [Cerambycidae], Mastigocera Dejean, 1835over Mallonia Thomson, 1857 [Cerambycidae], Zygocera Dejean, 1835 over Disternopsis Breuning, 1939 [Cerambycidae], Australica Chevrolat, 1836 over Calomela Hope, 1840 [Chrysomelidae], Edusa Chevrolat, 1836 over Edusella Chapuis, 1874 [Chrysomelidae], Litosonycha Chevrolat, 1836 over Asphaera Duponchel and Chevrolat, 1842 [Chrysomelidae], and Pleuraulaca Chevrolat, 1836 over Iphimeis Baly, 1864 [Chrysomelidae]. In each of these cases, Reversal of Precedence (ICZN 1999: 23.9) or an applicationto the International Commission on Zoological Nomenclature will be necessary to retain usage of the younger synonyms.     

Genotoxic and mutagenic effects of lipid-coated CdSe/ZnS quantum dots

We proposed to evaluate the genotoxicity and mutagenicity of a new quantum dots (QDs) nanoplatform (QDsN), consisting of CdSe/ZnS core–shell QDs encapsulated by a natural fusogenic lipid (1,2-di-oleoyl-sn-glycero-3-phosphocholine (DOPC)) and functionalized by a nucleolipid N-[5′-(2′,3′-di-oleoyl) uridine]-N′,N′,N′-trimethylammoniumtosylate (DOTAU). This QDs nanoplatform may represent a new therapeutic tool for the diagnosis and treatment of human cancers. The genotoxic, mutagenic and clastogenic effects of QDsN were compared to those of cadmium chloride (CdCl₂). Three assays were used: (1) the Salmonella/microsome assay with four tester strains, (2) the comet assay and (3) the micronucleus test on CHO cells. The contribution of simulated sunlight was studied in the three assays while oxidative events were only explored in the comet assay in aliquots pretreated with the antioxidant l-ergothioneine. We found that QDsN could enter CHO-K1 cells and accumulate in cytoplasmic vesicles. It was not mutagenic in the Salmonella/mutagenicity test whereas CdCl₂ was weakly positive. In the dark, both the QDsN and CdCl₂ similarly induced dose-dependent increases in single-strand breaks and micronuclei. Exposure to simulated sunlight significantly potentiated the genotoxic activities of both QDsN and CdCl₂, but did not significantly increase micronucleus frequencies. l-Ergothioneine significantly reduced but did not completely suppress the DNA-damaging activity of QDsN and CdCl₂. The present results clearly point to the genotoxic properties and the risk of long-term adverse effects of such a nanoplatform if used for human anticancer therapy and diagnosis in the future.     

Arv1 Regulates PM and ER Membrane Structure and Homeostasis But is Dispensable for Intracellular Sterol Transport

The pan‐eukaryotic endoplasmic reticulum (ER) membrane protein Arv1 has been suggested to play a role in intracellular sterol transport. We tested this proposal by comparing sterol traffic in wild‐type and Arv1‐deficient Saccharomyces cerevisiae. We used fluorescence microscopy to track the retrograde movement of exogenously supplied dehydroergosterol (DHE) from the plasma membrane (PM) to the ER and lipid droplets and high performance liquid chromatography to quantify, in parallel, the transport‐coupled formation of DHE esters. Metabolic labeling and subcellular fractionation were used to assay anterograde transport of ergosterol from the ER to the PM. We report that sterol transport between the ER and PM is unaffected by Arv1 deficiency. Instead, our results indicate differences in ER morphology and the organization of the PM lipid bilayer between wild‐type and arv1Δ cells suggesting a distinct role for Arv1 in membrane homeostasis. In arv1Δ cells, specific defects affecting single C‐terminal transmembrane domain proteins suggest that Arv1 might regulate membrane insertion of tail‐anchored proteins involved in membrane homoeostasis .     

Impact of bone marrow-derived mesenchymal stromal cells on experimental xenogeneic graft-versus-host disease

Background aimsGraft-versus-host disease (GVHD) is a life-threatening complication of allogeneic hematopoietic cell transplantation caused by donor T cells reacting against host tissues. Previous studies have suggested that mesenchymal stromal cells (MSCs) could exert potent immunosuppressive effects.MethodsThe ability of human bone marrow derived MSCs to prevent xenogeneic GVHD in non-obese diabetic/severe combined immunodeficient (NOD/SCID) mice and in NOD/SCID/interleukin-2Rγ(null) (NSG) mice transplanted with human peripheral blood mononuclear cells (PBMCs) was assessed.ResultsInjection of 200 × 10⁶ human PBMCs intraperitoneally (IP) into sub-lethally (3.0 Gy) irradiated NOD/SCID mice also given anti-asialo GM₁ antibodies IP 1 day prior and 8 days after transplantation induced lethal xenogeneic GVHD in all tested mice. Co-injection of 2 × 10⁶ MSCs IP on day 0 did not prevent lethal xenogeneic GVHD induced by injection of human PBMCs. Similarly, injection of 30 × 10⁶ human PBMCs IP into sub-lethally (2.5 Gy) irradiated NSG mice induced a lethal xenogeneic GVHD in all tested mice. Injection of 3 × 10⁶ MSCs IP on days 0, 7, 14 and 21 did not prevent lethal xenogeneic GVHD induced by injection of human PBMCs.ConclusionsInjection of MSCs did not prevent xenogeneic GVHD in these two humanized mice models.