Bottom‐up effect of host plants on life‐history characteristics of Aphidoletes aphidimyza feeding on Aphis gossypii

The predatory midge Aphidoletes aphidimyza (Rondani) (Diptera: Cecidomyiidae) is widely used for the control of Aphis spp. in many agricultural systems. We aimed to determine the most suitable host plant for rearing the predatory midges on the prey Aphis gossypii Glover (Hemiptera: Aphididae). Six host plants were selected: cucumber (Cucumis sativus L. cv. Beith Alpha), tomato (Solanum lycopersicum L. cv. Falat111), eggplant (Solanum melongena L. cv. Yummy), pepper (Capsicum annuum L. cv. Bertene) (all Solanaceae), okra [Abelmoschus esculentus (L.) Moensch cv. Clemson Spineless] (Malvaceae), and squash (Cucurbita pepo L. cv. Hybrid rajai) (Cucurbitaceae). Some physical traits (length and density of trichomes) and chemical attributes (nitrogen content) of prey host plants were investigated. The results showed that prey host plants differed significantly in their effect on fitness of the predator. The shortest immature development time (18.07 ± 0.257 days), the longest female adult longevity (7.5 ± 0.18 days), and the highest fecundity (89 eggs/female) of A. aphidimyza were found with squash as prey food. The highest intrinsic rate of increase (0.171 ± 0.009 day^?1) and also the shortest mean generation time (22.4 ± 0.32 days) were also obtained when A. aphidimyza fed on A. gossypii reared on squash. Canonical correlation analysis (CCA) approved the correlation between life‐history traits of A. aphidimyza and characteristics of prey host plants. The suitability of squash for rearing A. aphidimyza can be attributed to the higher nitrogen content, longer trichomes, and relatively high density of trichomes, which provided a better environment for A. gossypii and indirectly favored A. aphidimyza. This study showed that squash is the most suitable host plant for rearing A. aphidimyza feeding on A. gossypii.     

G protein beta gamma subunits inhibit nongenomic progesterone-induced signaling and maturation in Xenopus laevis oocytes. Evidence for a release of inhibition mechanism for cell cycle progression

Progesterone-induced maturation of Xenopus oocytes is a well known example of nongenomic signaling by steroids; however, little is known about the early signaling events involved in this process. Previous work has suggested that G proteins and G protein-coupled receptors may be involved in progesterone-mediated oocyte maturation as well as in other nongenomic steroid-induced signaling events. To investigate the role of G proteins in nongenomic signaling by progesterone, the effects of modulating Galpha and Gbetagamma levels in Xenopus oocytes on progesterone-induced signaling and maturation were examined. Our results demonstrate that Gbetagamma subunits, rather than Galpha, are the principal mediators of progesterone action in this system. We show that overexpression of Gbetagamma inhibits both progesterone-induced maturation and activation of the MAPK pathway, whereas sequestration of endogenous Gbetagamma subunits enhances progesterone-mediated signaling and maturation. These data are consistent with a model whereby endogenous free Xenopus Gbetagamma subunits constitutively inhibit oocyte maturation. Progesterone may induce maturation by antagonizing this inhibition and therefore allowing cell cycle progression to occur. These studies offer new insight into the early signaling events mediated by progesterone and may be useful in characterizing and identifying the membrane progesterone receptor in oocytes.     

4-(4-Chloro-2-methylphenoxy)-N-hydroxybutanamide (CMH) targets mRNA of the c-FLIP variants and induces apoptosis in MCF-7 human breast cancer cells

Cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein (c-FLIP) is a major resistance factor for the tumor necrosis factor-related apoptosis-inducing ligand TRAIL and in drug resistance in human malignancies. c-FLIP is an antagonist of caspases-8 and -10, which inhibits apoptosis and is expressed as long (c-FLIP_L) and short (c-FLIP_S) splice forms. c-FLIP is often overexpressed in various human cancers, including breast cancer. Several studies have shown that silencing c-FLIP by specific siRNAs sensitizes cancer cells to TRAIL and anticancer agents. However, systemic use of siRNA as a therapeutic agent is not practical at present. In order to reduce or inhibit c-FLIP expression, small molecules are needed to allow targeting c-FLIP without inhibiting caspases-8 and -10. We used a small molecule inhibitor of c-FLIP, 4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide (CMH), and show that CMH, but not its inactive analog, downregulated c-FLIP_L and c-FLIP_S mRNA and protein levels, caused poly(ADP-ribose) polymerase (PARP) degradation, reduced cell survival, and induced apoptosis in MCF-7 breast cancer cells. These results revealed that c-FLIP is a critical apoptosis regulator that can serve as a target for small molecule inhibitors that downregulate its expression and serve as effective targeted therapeutics against breast cancer cells.     

Bioprocess engineering of <Emphasis Type="Italic">Echium italicum</Emphasis> L.: induction of shikonin and alkannin derivatives by two-liquid-phase suspension cultures

An in vitro cell suspension culture of Echium italicum was established and assayed for the production of shikonin and alkannin derivatives. Callus tissues were induced from cotyledon explants of the plant incubated onto the solidified B5 medium. A two-liquid-phase system suspension culture was then established to elicit pigments of shikonin and alkannin derivatives using liquid paraffin. The presence of liquid paraffin efficiently induced production of pigments in cultured cells. The production and/or accumulation of these compounds in the E. italicum cells was examined using fluorescence microscopy as the naphthoquinone molecules display autofluorescent properties. Phytochemical analysis of the n-hexane extract of the medium was also carried out using preparative HPLC. The chemical structure of shikonin and alkannin derivatives were characterized by UV, 1H-NMR, and 13C-NMR techniques. Based on our findings, this bioprocess engineering approach resulted in induction of shikonin and alkannin derivatives, whereupon it may be recruited for production of these important secondary metabolites.     

Predation rate and numerical response of Aphidoletes aphidimyza feeding on different densities of Aphis craccivora

Predation rate and numerical response are basic to any investigation of predator–prey relationships and key components in the selection of predators for biological control. The density-dependent predation rate and numerical response of Aphidoletes aphidimyza (Rondani) (Diptera: Cecidomyiidae) to varying densities (5, 10, 20, 40, 60 and 80) of third-instar Aphis craccivora (Koch) (Hemiptera: Aphididae), were studied in laboratory conditions [23±1°C, 70 ± 5% relative humidity (RH), and a photoperiod of 16:8 h L:D. Predation rate data were analysed using the age-stage, two-sex consumption rate software. Net consumption rate (C₀) increased by increasing prey density. The lowest and highest net consumption rates were 20.75 and 190.8 prey nymphs at densities of 5 and 80 A. craccivora. The transformation rate from prey population to predator offspring (Q_p) increased by increasing prey density. The reproductive numerical response, in terms of eggs laid, increased curvilinearly with increasing prey density. Females laid 121.375 ± 4.301 eggs when exposed to the highest prey density (80) and 52.5 ± 1.544 eggs at lowest prey density (5). It can be concluded that different densities of A. craccivora influenced the reproductive performance of A. aphidimyza in terms of predation rate and numerical response.     

The influence of peroxisome proliferator-activated receptor γ(1) during differentiation of mouse embryonic stem cells to neural cells

Peroxisome proliferator activated receptor γ, belongs to PPARs, which exerts various metabolic functions including differentiation process. To testify the importance of PPARγ in neural differentiation of mouse embryonic stem cells (mESCs), its expression level was assessed. Data revealed an elevation in expression level of PPARγ when neural precursors (NPs) are formed upon retinoic acid treatment. Thus, involvement of PPARγ in two stages of neural differentiation of mESCs, during and post-NPs formation was examined by application of its agonist and antagonist. Our results indicated that PPARγ inactivation via treatment with GW9662 during NPs formation, reduced expression of neural precursor and neural (neuronal and astrocytes) markers. However, PPARγ inactivation by antagonist treatment post-NPs formation stage only decreased the expression of mature astrocyte marker (Gfap) suggesting that inactivation of PPARγ by antagonist decreased astrocyte differentiation. Here, we have demonstrated the stage dependent role of PPARγ modulation on neural differentiation of mESCs by retinoic acid treatment for the first time.