Insect- Host Plant-Parasitoid Interactions : SORGHUM MIDGE Contarlnla sorghicola (Coqulllett)

Three resistant (ICSV 745, ICSV 89058 and IS 10712) and three susceptible (Swarna, CSH 9 and ICSV 112) sorghum genotypes were sown on three dates each during the rainy (6, 15 and 30 Jul in rainy season 1992 and 2, 19 Jul and 6 Aug in rainy season 1993) and post-rainy (29 Oct, 13 Nov and 1 Dec 1992) seasons of 1992193. A modified headcage was developed for easy and precise collection of emerging insects. The species composition of natural enemies included three larval parasitoids (Aprostocetus sp., Eupelmus sp. and Apanfeles sp.) and one predator (Orius sp.). Parasitoid emergence commenced 1 - 3 weeks after initiation of midge emergence. The population dynamics of Aprostocetus sp, was similar in susceptible and resistant genotypes. Aprostocetus sp, activity was higher in the first and third sowing dates than in the second and greater numbers were recovered from susceptible than from resistant genotypes. The extent of parasitization of midge larvae did not follow a definite pattern with resistance or susceptibility of the host plant to midge. The lowest levels of parasitization were recorded from midge resistant ICSV 745. Studies on the tritrophic interactions indicated variations in preference for host stage for parasitization and development in rainy and post-rainy season

A simple head cage technique for monitoring sorghum midge (Diptera: Cecidomyiidae)

A head cage technique for monitoring populations of Stenodiplosis sorghicola, a variant of the type previously described for screening sorghum genotypes for resistance, was developed. The technique was effective and efficient in collecting adults from flowering sorghum panicles under field conditions in Andhra Pradesh, India. Adults emerged over 2-3 weeks during the 1992-93 post-rainy and 1-2 weeks during the 1993 rainy season. The activity (density) of S. sorghicola was higher during the rainy than during the post-rainy seaso

Tritrophic interactions in sorghum, midge (Stenodiplosis sorghicola) and its parasitoid (Aprostocetus spp.)

Studies were conducted on tritrophic interactions involving sorghum genotypes, Stenodiplosis sorghicola and the predominant parasitoids (Aprostocetus spp.) in Patancheru, Andhra Pradesh, India, using three midge resistant (ICSV 745, ICSV 89058 and IS 10712) and three susceptible (Swarna, CSH 9 and ICSV 112) genotypes during the post-rainy (1992/93) and rainy (1993) seasons. A. coimbatorensis, the predominant parasitoid during post-rainy season, preferred mid-late midge larvae for parasitization, while A. gala, which was predominant during the rainy season, preferred early-mid larval stages. Variations in the preference of A. coimbatorensis and A. gala for the developmental stage of their host larvae indicated good prospects for the biological control of sorghum midge populations. There were significant differences in parasitization level of midge by Aprostocetus spp. between resistant and susceptible sorghum genotypes, and season. Higher parasitization was observed on susceptible genotypes than on resistant ones during both post-rainy and rainy seasons. However, the level of parasitization was greater in post-rainy than in rainy seasons. There was also evidence of higher midge infestation in rainy than in post-rainy seasons. Susceptible genotypes attracted more parasitoids because of high levels of midge infestations. Low parasitoid density in midge resistant sorghum under glasshouse and field conditions was associated with low midge infestations in these genotypes. However, parasitoids were always associated with their host in spite of low midge densities in resistant genotypes. The present study revealed that the interaction between host plant resistance and parasitoids of sorghum midge would thus be synergistic and complementary and could result in successful integration of these two important pest management tactics

Emergence pattern of sorghum midge and its major parasitoids on midge-resistant and susceptible genotypes

Studies were conducted on the species composition of parasitoids of Stenodiplosis sorghicola, emergence pattern and level of parasitism. The studies were carried out in Andhra Pradesh, India, with three midge-resistant (ICSV 745, ICSV 89058 and IS 10712) and three susceptible (Swarna, CSH 9 and ICSV 112) sorghum genotypes during the 1992-93 post-rainy and 1993 rainy seasons. The species of parasitoids collected were Aprostocetus gala, A. coimbatorensis and Eupelmus spp. The species composition varied with the season, but was unaffected by varietal resistance and susceptibility to the midge. Although both species of Aprostocetus were present in rainy and post-rainy seasons, A. gala was predominant during the rainy season whereas A. Coimbatorensis was predominant in the post-rainy season. There was no significant difference in the pattern of parasitoid emergence or the level of midge parasitization between resistant and susceptible genotypes. These results indicate that resistance to midge in the genotypes studied was not antagonistic to parasitoid activity, and that there is potential to interface biological control with host-plant resistance in the management of this insect

Kupffer Cells Hasten Resolution of Liver Immunopathology in Mouse Models of Viral Hepatitis

Kupffer cells (KCs) are widely considered important contributors to liver injury during viral hepatitis due to their pro-inflammatory activity. Herein we utilized hepatitis B virus (HBV)-replication competent transgenic mice and wild-type mice infected with a hepatotropic adenovirus to demonstrate that KCs do not directly induce hepatocellular injury nor do they affect the pathogenic potential of virus-specific CD8 T cells. Instead, KCs limit the severity of liver immunopathology. Mechanistically, our results are most compatible with the hypothesis that KCs contain liver immunopathology by removing apoptotic hepatocytes in a manner largely dependent on scavenger receptors. Apoptotic hepatocytes not readily removed by KCs become secondarily necrotic and release high-mobility group box 1 (HMGB-1) protein, promoting organ infiltration by inflammatory cells, particularly neutrophils. Overall, these results indicate that KCs resolve rather than worsen liver immunopathology

Functional annotations of diabetes nephropathy susceptibility loci through analysis of genome-wide renal gene expression in rat models of diabetes mellitus

<p>Abstract</p> <p>Background</p> <p>Hyperglycaemia in diabetes mellitus (DM) alters gene expression regulation in various organs and contributes to long term vascular and renal complications. We aimed to generate novel renal genome-wide gene transcription data in rat models of diabetes in order to test the responsiveness to hyperglycaemia and renal structural changes of positional candidate genes at selected diabetic nephropathy (DN) susceptibility loci.</p> <p>Methods</p> <p>Both Affymetrix and Illumina technologies were used to identify significant quantitative changes in the abundance of over 15,000 transcripts in kidney of models of spontaneous (genetically determined) mild hyperglycaemia and insulin resistance (Goto-Kakizaki-GK) and experimentally induced severe hyperglycaemia (Wistar-Kyoto-WKY rats injected with streptozotocin [STZ]).</p> <p>Results</p> <p>Different patterns of transcription regulation in the two rat models of diabetes likely underlie the roles of genetic variants and hyperglycaemia severity. The impact of prolonged hyperglycaemia on gene expression changes was more profound in STZ-WKY rats than in GK rats and involved largely different sets of genes. These included genes already tested in genetic studies of DN and a large number of protein coding sequences of unknown function which can be considered as functional and, when they map to DN loci, positional candidates for DN. Further expression analysis of rat orthologs of human DN positional candidate genes provided functional annotations of known and novel genes that are responsive to hyperglycaemia and may contribute to renal functional and/or structural alterations.</p> <p>Conclusion</p> <p>Combining transcriptomics in animal models and comparative genomics provides important information to improve functional annotations of disease susceptibility loci in humans and experimental support for testing candidate genes in human genetics.</p

Organization of multiprotein complexes at cell–cell junctions

The formation of stable cell–cell contacts is required for the generation of barrier-forming sheets of epithelial and endothelial cells. During various physiological processes like tissue development, wound healing or tumorigenesis, cellular junctions are reorganized to allow the release or the incorporation of individual cells. Cell–cell contact formation is regulated by multiprotein complexes which are localized at specific structures along the lateral cell junctions like the tight junctions and adherens junctions and which are targeted to these site through their association with cell adhesion molecules. Recent evidence indicates that several major protein complexes exist which have distinct functions during junction formation. However, this evidence also indicates that their composition is dynamic and subject to changes depending on the state of junction maturation. Thus, cell–cell contact formation and integrity is regulated by a complex network of protein complexes. Imbalancing this network by oncogenic proteins or pathogens results in barrier breakdown and eventually in cancer. Here, I will review the molecular organization of the major multiprotein complexes at junctions of epithelial cells and discuss their function in cell–cell contact formation and maintenance

Tight junctions and the modulation of barrier function in disease

Tight junctions create a paracellular barrier in epithelial and endothelial cells protecting them from the external environment. Two different classes of integral membrane proteins constitute the tight junction strands in epithelial cells and endothelial cells, occludin and members of the claudin protein family. In addition, cytoplasmic scaffolding molecules associated with these junctions regulate diverse physiological processes like proliferation, cell polarity and regulated diffusion. In many diseases, disruption of this regulated barrier occurs. This review will briefly describe the molecular composition of the tight junctions and then present evidence of the link between tight junction dysfunction and disease

Environmentally Realistic Exposure to the Herbicide Atrazine Alters Some Sexually Selected Traits in Male Guppies

Male mating signals, including ornaments and courtship displays, and other sexually selected traits, like male-male aggression, are largely controlled by sex hormones. Environmental pollutants, notably endocrine disrupting compounds, can interfere with the proper functioning of hormones, thereby impacting the expression of hormonally regulated traits. Atrazine, one of the most widely used herbicides, can alter sex hormone levels in exposed animals. I tested the effects of environmentally relevant atrazine exposures on mating signals and behaviors in male guppies, a sexually dimorphic freshwater fish. Prolonged atrazine exposure reduced the expression of two honest signals: the area of orange spots (ornaments) and the number of courtship displays performed. Atrazine exposure also reduced aggression towards competing males in the context of mate competition. In the wild, exposure levels vary among individuals because of differential distribution of the pollutants across habitats; hence, differently impacted males often compete for the same mates. Disrupted mating signals can reduce reproductive success as females avoid mating with perceptibly suboptimal males. Less aggressive males are at a competitive disadvantage and lose access to females. This study highlights the effects of atrazine on ecologically relevant mating signals and behaviors in exposed wildlife. Altered reproductive traits have important implications for population dynamics, evolutionary patterns, and conservation of wildlife species

Claudins in renal physiology and disease

The tight junction forms the paracellular permeability barrier in all epithelia, including the renal tubule. Claudins are a family of tight junction membrane proteins with four transmembrane domains that form the paracellular pore and barrier. Their first extracellular domain appears to be important for determining selectivity. A number of claudin isoforms have been found to be important in renal tubule function, both in adults and in neonates. Familial hypomagnesemic hypercalciuria with nephrocalcinosis is an autosomal recessive syndrome characterized by impaired reabsorption of Mg and Ca in the thick ascending limb of Henle's loop. Mutations in claudin-16 and 19 can both cause this syndrome, but the pathophysiological mechanism remains controversial