Molecular phylogeny and historical biogeography of the Anatolian lizard Apathya (Squamata,Lacertidae)

Apathya is a lacertid genus occurring mainly in south-east Turkey and its adjacent regions (part of Iran and Iraq). So far two morphological species have been attributed to the genus; A. cappadocica (with five subspecies, A. c. cappadocica, A. c. muhtari, A. c. schmidtlerorum, A. c. urmiana and A. c. wolteri) and A. yassujica. The first species occupies most of the genus’ distribution range, while A. yassujica is endemic of the Zagros Mountains. Here, we explored Apathya’s taxonomy and investigated the evolutionary history of the species by employing phylogenetic and phylogeographic approaches and using both mitochondrial (mtDNA) and nuclear markers. The phylogenetic relationships and the genetic distances retrieved, revealed that Apathya is a highly variable genus, which parallels its high morphological variation. Such levels of morphological and genetic differentiation often exceed those between species of other Lacertini genera that are already treated as full species, suggesting the necessity for a taxonomic revision of Apathya. The phylogeographical scenario emerging from the genetic data suggests that the present distribution of the genus was determined by a combination of dispersal and vicariance events between Anatolia and Southwest Asia dating back to the Miocene and continuing up to the Pleistocene. Key geological events for the understanding of the phylogeography of the genus are the movement of the Arabian plate that led to the configuration of Middle East (orogenesis of the mountain ranges of Turkey and Iran) and the formation of Anatolian Diagonal.     

Phylogenetic relationships of the populations of Iranolacerta brandtii (de Filippi, 1863) (Squamata: Lacertidae) recently found in Eastern Anatolia,Turkey

The Persian Lizard, Iranolacerta brandtii, was until recently considered to be restricted to north-western Iran (Azerbaijan and Esfahan provinces). However, two recent studies have revealed the existence of populations in Eastern Anatolia, extending the range of this species for about 230?km westwards. The fragmented distribution of this species has been considered to be a consequence of the climatic oscillations during the Pleistocene and Holocene, which created events of alternating contact and isolation of populations in distinct glacial refugia. According to our obtained genealogy derived from three mitochondrial fragments (12S rRNA, 16S rRNA and cytb), the Turkish specimens cluster together but form an independent clade, sister to the individuals from Tabriz in Iran. The separation of these two clades is concurrent with the cladogenesis between the Esfahan and Ardabil clades, estimated to have taken place during the late Holocene.     

Rac1 and Toll-IL-1 receptor domain-containing adapter protein mediate Toll-like receptor 4 induction of HIV-long terminal repeat

Opportunistic infections, common in HIV-1-infected patients, increase HIV replication; however, the intracellular signaling mechanisms involved are not clearly known. We have shown that Toll-like receptor 2 (TLR2), TLR4, and TLR9 mediate microbial Ag-induced HIV-long terminal repeat (HIV-LTR) trans-activation and HIV-1 replication, and that LPS-induced HIV-LTR trans-activation is mediated through myeloid differentiation adapter protein. Recently, Toll-IL-1R domain-containing adapter protein (TIRAP) has been identified as an adapter molecule that mediates responses to TLR2 and TLR4 ligands, and TIRAP was suggested to provide signaling specificity for different TLRs. Rac1, a small GTP-binding protein that is activated upon LPS stimulation of macrophages, activates phosphatidylinositol 3-kinase and Akt and leads to NF-kappaB activation. The roles of Rac1 and TIRAP in LPS activation of HIV replication is not known. In the present study we show that LPS stimulation of human microvessel endothelial cells leads to Rac1 activation. Constitutively active Rac1 (Rac1V12) simulated the effect of LPS to activate HIV-LTR, whereas the expression of dominant negative Rac1 (Rac1N17) partially blocked LPS-induced HIV-LTR trans-activation. Rac1V12-induced HIV-LTR activation was independent of myeloid differentiation adapter protein, and dominant negative TIRAP blocked Rac1V12-induced HIV-LTR trans-activation. In this study we show for the first time that activation of Rac1 leads to HIV-LTR trans-activation, and this is mediated through TIRAP. Together these results underscore the importance of Rac1 and TIRAP in TLR4 activation of HIV replication and help delineate the signaling pathways induced by TLRs to mediate microbial Ag-induced HIV replication and HIV pathogenesis.     

Eicosanoids mediate melanotic nodulation reactions to viral infection in larvae of the parasitic wasp, Pimpla turionellae

Nodulation is the quantitatively predominant insect cellular immune function activated in response to bacterial, fungal and some viral infections. We posed the hypothesis that parasitoid insects express melanotic nodulation reactions to viral challenge and that eicosanoids mediate these reactions. Treating fifth-instar larvae of the ichneumonid endoparasitoid Pimpla turionellae with Bovine Herpes Simplex Virus-1 (BHSV-1) induced nodulation reactions in a challenge dose-dependent manner. Experimental larvae treated with the cyclooxygenase inhibitor, indomethacin, the lipoxygenase inhibitor, esculetin, and the phospholipase A2 inhibitor, dexamethasone, resulted in severely impaired nodulation reactions to our standard BHSV-1 challenge dose. The immunoinhibitory influence of dexamethasone was reversed in larvae reared on culture medium amended with arachidonic acid, the fatty acid precursor of eicosanoid biosynthesis. Larvae that had been reared on media amended with indomethacin, esculetin, or dexamethasone were also compromised in their nodulation reactions to viral challenge. The influence of the orally administered pharmaceutical was expressed in a dose-dependent manner. Finally, wasp larvae reared in the presence of indomethacin and dexamethasone expressed significantly decreased levels of phenoloxidase activity in response to viral challenge. These findings draw attention to the idea that endoparasitoid insects express cellular immune reactions to viral challenge; they also support our hypothesis that eicosanoids mediate nodulation reactions to viral challenge in these highly specialized insects.     

Biological and immune response of Galleria mellonella (Lepidoptera: Pyralidae) to sodium tetraborate

Inorganic insecticides are commonly used in urban pest management because of their low mammalian toxicity. We tested the effects of sodium tetraborate (ST) on life parameters of greater wax moth, Galleria mellonella (L.) (Lepidoptera: Pyralidae), to determine its sublethal toxicity on the insect. Survival, development, adult longevity, and fecundity of the wax moth were investigated by rearing larvae on artificial diets containing ST at concentrations of 0.005, 0.1, 0.2, or 0.3%. Larvae reared on medium at the highest concentration of ST (0.3%) had significantly decreased survival to the seventh instar and prolonged time required to reach the seventh instar. This concentration reduced pupa and adult yields to 12.5%, and it also prolonged development by 5 d. ST did not significantly influence adult longevity. Dietary ST led to significant decreases in fecundity and egg viability. Oviposition of survivors at the highest ST concentration (0.3%) was completely inhibited. Lysozyme content was decreased in larval hemolymph and fat body at high dietary ST concentrations. Fat body lysozyme content was significantly increased two-fold for larvae reared on diet at the lowest concentration of ST (0.005%). However, the highest concentration (0.3%) dramatically decreased fat body lysozyme content from 0.12 +/- 0.013 to 0.006 +/- 0.003 mg/ml in seventh instars. We infer that sublethal levels of dietary ST substantially influence life history parameters and immunocompetence in G. mellonella.     

Saposin Lipid Nanoparticles: A Highly Versatile and Modular Tool for Membrane Protein Research

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24-Epibrassinolide ameliorates the effects of boron toxicity on <Emphasis Type="Italic">Arabidopsis thaliana</Emphasis> (L.) Heynh by activating an antioxidant system and decreasing boron accumulation

Brassinosteroids (BRs) play a significant role in alleviating the negative effects of various environmental stresses and in promoting the growth and development of plants. In this study, we investigated the effects of 24-epibrassinolide (EBL) on the growth, boron (B) accumulation and activation of the antioxidant system of Arabidopsis thaliana (L.) Heynh exposed to high concentrations of boric acid (BA). A. thaliana plants were grown in a hydroponic culture, and after 4 weeks, the plants were transferred to media containing either 0.80 or 1.60 mM BA. Following BA treatment, 0.01 and 1 µM EBL was sprayed on the entire foliar region of the seedlings. B toxicity induced oxidative stress and considerably inhibited the growth of the plants. The spraying of EBL on the B-treated plants resulted in increases in growth (both fresh and dry shoot mass, silique number, length and mass) and pigment content (total chlorophyll and carotenoids). Excessive B levels increased the activities of antioxidant enzymes, including superoxide dismutase, catalase, ascorbate peroxidase, and guaiacol peroxidase, and increased the proline content in leaves of plants. However, treatment of the B-stressed plants with EBL further enhanced the activities of the antioxidant enzymes and increased the content of proline. The high level of lipid peroxidation in plants observed during exposure to a higher level of BA was decreased following EBL treatment. Thus, this study showed that the exogenous application of EBL ameliorates the toxic effects of B in a model plant by improving the plant’s antioxidant system and decreasing B accumulation. To our knowledge, this is the one of the first studies to examine the effect of BR in plants subjected to B toxicity.     

MyD88 is pivotal for the early inflammatory response and subsequent bacterial clearance and survival in a mouse model of Chlamydia pneumoniae pneumonia

Chlamydia pneumoniae is the causative agent of respiratory tract infections and a number of chronic diseases. Here we investigated the involvement of the common TLR adaptor molecule MyD88 in host responses to C. pneumoniae-induced pneumonia in mice. MyD88-deficient mice were severely impaired in their ability to mount an acute early inflammatory response toward C. pneumoniae. Although the bacterial burden in the lungs was comparable 5 days after infection, MyD88-deficient mice exhibited only minor signs of pneumonia and reduced expression of inflammatory mediators. MyD88-deficient mice were unable to up-regulate proinflammatory cytokines and chemokines, demonstrated delayed recruitment of CD8+ and CD4+ T cells to the lungs, and were unable to clear the pathogen from their lungs at day 14. At day 14 the MyD88-deficent mice developed a severe, chronic lung inflammation with elevated IL-1beta and IFN-gamma leading to increased mortality, whereas wild-type mice as well as TLR2- or TLR4-deficient mice recovered from acute pneumonia and did not show delayed bacterial clearance. Thus, MyD88 is essential to recognize C. pneumoniae infection and initiate a prompt and effective immune host response against this organism leading to clearance of bacteria from infected lungs.