Characterization of Cry IIa Transgenic Chickpea Lines and their Interaction with Natural Enemies of Helicoverpa armigera(Hubner)

The present research on the “Characterization of Cry IIa transgenic chickpea lines and their interaction with natural enemies of Helicoverpa armigera (Hubner)” was carried out under laboratory and field conditions at the International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), Patancheru, Andhra Pradesh, India, during 2011 – 14. The transgenic plants suffered significantly lower leaf damage as compared to the non-transgenic plants. The larval survival and weight gained by H. armigera larvae after 5 days was significantly reduced on transgenic lines as compared to that on non-transgenic chickpeas during October and November plantings 2011-12 and 2012-13. The transgenic lines BS5A.2(T2) 19-1P2 and BS5A.2(T2) 19-2P1 exhibited significantly lower leaf damage rating, larval survival and mean larval weight under laboratory conditions. In glasshouse conditions, BS5A.1(T2) 18-1P1 suffered significantly lower leaf damage and mean larval weight was also reduced but the larval survival of H. armigera was significantly reduced on BS5A.2(T2) 19-2P1. Significant differences in grain yield were observed between transgenic and non-transgenic plants infested with H. armigera. BS5A.2(T2) 19-2P1 had the highest dry matter weight, pod weight, seed weight and number of seeds formed as compared to the other transgenic and non-transgenic chickpea lines under infested and un-infested conditions..

Effect of CryIIa transgenic chickpeas to Helicoverpa armigera larval parasitoid, Campoletis chlorideae

The current experiments were conducted to evaluate the effect of transgenic chickpea lines expressing CryIIa to C. chlorideae under laboratory conditions. There was a significant reduction in cocoon formation and adult emergence of C. chlorideae reared on H. armigera larvae fed on the leaves of transgenic chickpea before and after parasitisation. The larval period was prolonged and was a significant difference between the transgenic and nontransgenic chickpea lines was observed. Although the pupal period of the parasitoid was prolonged, there were no significant differences between the transgenic and nontransgenic chickpea lines. The adverse effects of transgenic chickpea lines on cocoon formation and adult emergence of C.chlorideae were largely due to the early mortality of H.armigera larvae, but there was no direct toxicity of Bt toxin protein to C. chlorideae. The amount of CryIIa protein transferred from leaves to the non-target insects and natural enemies were negligible

Evaluation of Cry IIa transgenic chickpea lines for resistance to Helicoverpa armigera (Hubner) using detached leaf assay

Studies were conducted to evaluate transgenic chickpea lines encoding Cry IIa for resistance to Helicoverpa armigera. Significantly lower leaf damage was noticed in transgenic chickpea lines when compared to non-transgenic lines. Significant reduction in larval survival and weight gain were observed when H. armigera were fed on transgenic lines under laboratory conditions. Across the seasons (2011-12 and 2012-13), the transgenic chickpea lines BS5A.2(T2) 19-1P2 and BS5A.2(T2) 19-2P1 showed enhanced levels of resistance to H. armigera

Direct effect of CryIIa transgenic chickpea on coccinellid, Cheilomenes sexmaculatus (Fabricius)

The experiments were conducted during 2012-2014 at ICRISAT, Hyderabad to study the direct effects of transgenic chickpea lines on coccinellid beetle, Cheilomenes sexmaculatus (Fabricius). The direct effects on coccinellids were greater when fed on 0.1% Bt intoxicated diet, followed by diets with 0.05% and 0.02% Bt. The survival and development of coccinellid grubs were slightly affected when reared on aphids fed on diets with different concentrations (0.02%, 0.05% and 0.1%) of transgenic chickpea leaf powder. The coccinellids fed on diets with 0.05% BS5A.2(T2) 19-3P1 leaf powder showed a marginal reduction in survival and development as compared to that on other transgenic lines

Control of the induction of type I interferon by Peste des petits ruminants virus.

Peste des petits ruminants virus (PPRV) is a morbillivirus that produces clinical disease in goats and sheep. We have studied the induction of interferon-β (IFN-β) following infection of cultured cells with wild-type and vaccine strains of PPRV, and the effects of such infection with PPRV on the induction of IFN-β through both MDA-5 and RIG-I mediated pathways. Using both reporter assays and direct measurement of IFN-β mRNA, we have found that PPRV infection induces IFN-β only weakly and transiently, and the virus can actively block the induction of IFN-β. We have also generated mutant PPRV that lack expression of either of the viral accessory proteins (V&C) to characterize the role of these proteins in IFN-β induction during virus infection. Both PPRV_ΔV and PPRV_ΔC were defective in growth in cell culture, although in different ways. While the PPRV V protein bound to MDA-5 and, to a lesser extent, RIG-I, and over-expression of the V protein inhibited both IFN-β induction pathways, PPRV lacking V protein expression can still block IFN-β induction. In contrast, PPRV C bound to neither MDA-5 nor RIG-I, but PPRV lacking C protein expression lost the ability to block both MDA-5 and RIG-I mediated activation of IFN-β. These results shed new light on the inhibition of the induction of IFN-β by PPRV

An Empirical Comparison of Consumer Innovation Adoption Models: Implications for Subsistence Marketplaces

So called “pro-poor” innovations may improve consumer wellbeing in subsistence marketplaces. However, there is little research that integrates the area with the vast literature on innovation adoption. Using a questionnaire where respondents were asked to provide their evaluations about a mobile banking innovation, this research fills this gap by providing empirical evidence of the applicability of existing innovation adoption models in subsistence marketplaces. The study was conducted in Bangladesh among a geographically dispersed sample. The data collected allowed an empirical comparison of models in a subsistence context. The research reveals the most useful models in this context to be the Value Based Adoption Model and the Consumer Acceptance of Technology model. In light of these findings and further examination of the model comparison results the research also shows that consumers in subsistence marketplaces are not just motivated by functionality and economic needs. If organizations cannot enhance the hedonic attributes of a pro-poor innovation, and reduce the internal/external constraints related to adoption of that pro-poor innovation, then adoption intention by consumers will be lower

A framework for human microbiome research

A variety of microbial communities and their genes (the microbiome) exist throughout the human body, with fundamental roles in human health and disease. The National Institutes of Health (NIH)-funded Human Microbiome Project Consortium has established a population-scale framework to develop metagenomic protocols, resulting in a broad range of quality-controlled resources and data including standardized methods for creating, processing and interpreting distinct types of high-throughput metagenomic data available to the scientific community. Here we present resources from a population of 242 healthy adults sampled at 15 or 18 body sites up to three times, which have generated 5,177 microbial taxonomic profiles from 16S ribosomal RNA genes and over 3.5 terabases of metagenomic sequence so far. In parallel, approximately 800 reference strains isolated from the human body have been sequenced. Collectively, these data represent the largest resource describing the abundance and variety of the human microbiome, while providing a framework for current and future studies

Structure, function and diversity of the healthy human microbiome

Author Posting. © The Authors, 2012. This article is posted here by permission of Nature Publishing Group. The definitive version was published in Nature 486 (2012): 207-214, doi:10.1038/nature11234.Studies of the human microbiome have revealed that even healthy individuals differ remarkably in the microbes that occupy habitats such as the gut, skin and vagina. Much of this diversity remains unexplained, although diet, environment, host genetics and early microbial exposure have all been implicated. Accordingly, to characterize the ecology of human-associated microbial communities, the Human Microbiome Project has analysed the largest cohort and set of distinct, clinically relevant body habitats so far. We found the diversity and abundance of each habitat’s signature microbes to vary widely even among healthy subjects, with strong niche specialization both within and among individuals. The project encountered an estimated 81–99% of the genera, enzyme families and community configurations occupied by the healthy Western microbiome. Metagenomic carriage of metabolic pathways was stable among individuals despite variation in community structure, and ethnic/racial background proved to be one of the strongest associations of both pathways and microbes with clinical metadata. These results thus delineate the range of structural and functional configurations normal in the microbial communities of a healthy population, enabling future characterization of the epidemiology, ecology and translational applications of the human microbiome.This research was supported in part by National Institutes of Health grants U54HG004969 to B.W.B.; U54HG003273 to R.A.G.; U54HG004973 to R.A.G., S.K.H. and J.F.P.; U54HG003067 to E.S.Lander; U54AI084844 to K.E.N.; N01AI30071 to R.L.Strausberg; U54HG004968 to G.M.W.; U01HG004866 to O.R.W.; U54HG003079 to R.K.W.; R01HG005969 to C.H.; R01HG004872 to R.K.; R01HG004885 to M.P.; R01HG005975 to P.D.S.; R01HG004908 to Y.Y.; R01HG004900 to M.K.Cho and P. Sankar; R01HG005171 to D.E.H.; R01HG004853 to A.L.M.; R01HG004856 to R.R.; R01HG004877 to R.R.S. and R.F.; R01HG005172 to P. Spicer.; R01HG004857 to M.P.; R01HG004906 to T.M.S.; R21HG005811 to E.A.V.; M.J.B. was supported by UH2AR057506; G.A.B. was supported by UH2AI083263 and UH3AI083263 (G.A.B., C. N. Cornelissen, L. K. Eaves and J. F. Strauss); S.M.H. was supported by UH3DK083993 (V. B. Young, E. B. Chang, F. Meyer, T. M. S., M. L. Sogin, J. M. Tiedje); K.P.R. was supported by UH2DK083990 (J. V.); J.A.S. and H.H.K. were supported by UH2AR057504 and UH3AR057504 (J.A.S.); DP2OD001500 to K.M.A.; N01HG62088 to the Coriell Institute for Medical Research; U01DE016937 to F.E.D.; S.K.H. was supported by RC1DE0202098 and R01DE021574 (S.K.H. and H. Li); J.I. was supported by R21CA139193 (J.I. and D. S. Michaud); K.P.L. was supported by P30DE020751 (D. J. Smith); Army Research Office grant W911NF-11-1-0473 to C.H.; National Science Foundation grants NSF DBI-1053486 to C.H. and NSF IIS-0812111 to M.P.; The Office of Science of the US Department of Energy under Contract No. DE-AC02-05CH11231 for P.S. C.; LANL Laboratory-Directed Research and Development grant 20100034DR and the US Defense Threat Reduction Agency grants B104153I and B084531I to P.S.C.; Research Foundation - Flanders (FWO) grant to K.F. and J.Raes; R.K. is an HHMI Early Career Scientist; Gordon&BettyMoore Foundation funding and institutional funding fromthe J. David Gladstone Institutes to K.S.P.; A.M.S. was supported by fellowships provided by the Rackham Graduate School and the NIH Molecular Mechanisms in Microbial Pathogenesis Training Grant T32AI007528; a Crohn’s and Colitis Foundation of Canada Grant in Aid of Research to E.A.V.; 2010 IBM Faculty Award to K.C.W.; analysis of the HMPdata was performed using National Energy Research Scientific Computing resources, the BluBioU Computational Resource at Rice University