RNA interference of NADPH-cytochrome P450 reductase increases susceptibilities to multiple acaricides in Tetranychus urticae.

The two-spotted spider mite, Tetranychus urticae, is a polyphagous pest feeding on over 1100 plant species, including numerous highly valued economic crops. The control of T. urticae largely depends on the use of acaricides, which leads to pervasive development of acaricide resistance.

Multiple insecticide resistance in onion thrips populations from Western USA.

Thrips tabaci is a key pest of onions, especially in the Pacific Northwestern USA. Management of T. tabaci is dominated by the application of various insecticides.

Cell Cycle Progression Determines Wing Morph in the Polyphenic Insect Nilaparvata lugens.

Wing polyphenism is a phenomenon in which one genotype can produce two or more distinct wing phenotypes adapted to the particular environment. What remains unknown is how wing pad development is controlled downstream of endocrine signals such as insulin and JNK pathways. We show that genes important in cellular proliferation, cytokinesis, and cell cycle progression are necessary for growth and development of long wings.

Physiological resistance alters behavioral response of Tetranychus urticae to acaricides.

Multiple acaricide resistance in Tetranychus urticae continues to threaten crop production globally, justifying the need to adequately study resistance for sustainable pest management. Most studies on acaricide resistance have focused on the acute contact toxicity of acaricides with little or no information on the behavioral responses elicited after acaricide exposure. Furthermore, the impact of physiological resistance on these behavioral responses remains unknown in most pest species, including T.

The Insulin Signaling Substrate Chico and the Ecdysone Response Element Broad Both Regulate Growth of the Head Horns in the Asian Rhinoceros Beetle, Trypoxylus dichotomus.

Males of the Asian rhinoceros beetle, Trypoxylus dichotomus, possess exaggerated head and thoracic horns that scale dramatically out of proportion to body size. While RNAi-mediated knockdowns of the insulin receptor suggest that the insulin signaling pathway regulates nutrition-dependent growth including exaggerated horns, the genes that regulate disproportionate growth have yet to be identified. We used RNAi-mediated knockdown of several genes to investigate their potential role in growth and scaling of the sexually dimorphic, exaggerated head horns of T.

The activin signaling transcription factor Smox is an essential regulator of appendage size during regeneration after autotomy in the crayfish.

Members of the phylum Arthropoda, comprising over 80% of total animal species, have evolved regenerative abilities, but little is known about the molecular mechanisms mediating this process. Transforming growth factor β (TGF-β) signaling mediates a diverse set of essential processes in animals and is a good candidate pathway for regulation of regeneration in arthropods. In this study we investigated the role of activin signaling, a TGF-β superfamily pathway, in limb regeneration in the crayfish.

The Fat-Dachsous signaling pathway regulates growth of horns in Trypoxylus dichotomus, but does not affect horn allometry.

Males of the Asian rhinoceros beetle, Trypoxylus dichotomus, possess exaggerated head and thoracic horns that scale dramatically out of proportion to body size. While studies of insulin signaling suggest that this pathway regulates nutrition-dependent growth including exaggerated horns, what regulates disproportionate growth has yet to be identified. The Fat signaling pathway is a potential candidate for regulating disproportionate growth of sexually-selected traits, a hypothesis we advanced in a previous paper (Gotoh et al.

A basic domain in the histone H2B N-terminal tail is important for nucleosome assembly by FACT.

Nucleosome assembly in vivo requires assembly factors, such as histone chaperones, to bind to histones and mediate their deposition onto DNA. In yeast, the essential histone chaperone FACT (FAcilitates Chromatin Transcription) functions in nucleosome assembly and H2A-H2B deposition during transcription elongation and DNA replication. Recent studies have identified candidate histone residues that mediate FACT binding to histones, but it is not known which histone residues are important for FACT to deposit histones onto DNA during nucleosome assembly.

Selection of Reference Genes for Expression Studies of Xenobiotic Adaptation in Tetranychus urticae.

Quantitative real-time PCR (qRT-PCR) is an extensively used, high-throughput method to analyze transcriptional expression of genes of interest. An appropriate normalization strategy with reliable reference genes is required for calculating gene expression across diverse experimental conditions. In this study, we aim to identify the most stable reference genes for expression studies of xenobiotic adaptation in Tetranychus urticae, an extremely polyphagous herbivore causing significant yield reduction of agriculture.

JNK signaling mediates wing form polymorphism in brown planthoppers (Nilaparvata lugens).

Wing polyphenism is considered to be an adaptive trade-off between migration (long winged forms) and reproduction (short winged forms), determined by various environmental conditions. The c-Jun NH2-terminal kinase (JNK) is crucial for the regulation of the activity of a number of transcription factors, and is activated under stress and environmental fluctuations where it functions in maintaining cell viability and proliferation. We used RNA interference and a pharmacological inhibitor of JNK to test the role of JNK signaling in regulating the wing dimorphism of the brown planthopper, Nilaparvata lugens.

FOXO links wing form polyphenism and wound healing in the brown planthopper, Nilaparvata lugens.

Polyphenisms such as wing dimorphisms and caste determination are important in allowing animals to adapt to changing environments. The brown planthopper Nilaparvata lugens, one of the most serious insect agricultural pests, includes two wing forms, the long wing form (macropterous) and the short wing form (brachypterous). Long wings are specialized for migration, while short wings are found in individuals specialized for reproduction.

Analysis of monensin sensitivity in Toxoplasma gondii reveals autophagy as a mechanism for drug induced death.

Understanding the mechanisms by which anti-parasitic drugs alter the physiology and ultimately kill is an important area of investigation. Development of novel parasitic drugs, as well as the continued utilization of existing drugs in the face of resistant parasite populations, requires such knowledge. Here we show that the anti-coccidial drug monensin kills Toxoplasma gondii by inducing autophagy in the parasites, a novel mechanism of cell death in response to an antimicrobial drug.

A novel benzodioxole-containing inhibitor of Toxoplasma gondii growth alters the parasite cell cycle.

Toxoplasma gondii is an obligate intracellular parasite that can cause disease in the developing fetus and in immunocompromised humans. Infections can last for the life of the individual, and to date there are no drugs that eliminate the chronic cyst stages that are characteristic of this parasite. In an effort to identify new chemical scaffolds that could form the basis for new therapeutics, we carried out a chemoinformatic screen for compounds that had the potential to interact with members of a superfamily of parasite-secreted kinases and assayed them for growth inhibition in vitro.

The antibiotic monensin causes cell cycle disruption of Toxoplasma gondii mediated through the DNA repair enzyme TgMSH-1.

Monensin is a polyether ionophore antibiotic that is widely used in the control of coccidia in animals. Despite its significance in veterinary medicine, little is known about its mode of action and potential mechanisms of resistance in coccidian parasites. Here we show that monensin causes accumulation of the coccidian Toxoplasma gondii at an apparent late-S-phase cell cycle checkpoint.

Induction of mitotic S-phase of host and neighboring cells by Toxoplasma gondii enhances parasite invasion.

The intracellular parasite Toxoplasma gondii extensively modifies its host cell so as to efficiently grow and divide. Among these cellular changes, T. gondii alters the cell cycle of host cells it has invaded.

Exit from host cells by the pathogenic parasite Toxoplasma gondii does not require motility.

The process by which the intracellular parasite Toxoplasma gondii exits its host cell is central to its propagation and pathogenesis. Experimental induction of motility in intracellular parasites results in parasite egress, leading to the hypothesis that egress depends on the parasite's actin-dependent motility. Using a novel assay to monitor egress without experimental induction, we have established that inhibiting parasite motility does not block this process, although treatment with actin-disrupting drugs does delay egress.

A Toxoplasma gondii mutant defective in responding to calcium fluxes shows reduced in vivo pathogenicity.

Toxoplasma gondii is an important opportunistic pathogen in immunocompromised individuals. Successful propagation in an infected host by this obligate intracellular parasite depends on its ability to enter and exit host cells. Egress from the cell can be artificially induced by causing fluxes of calcium within the parasite with the use of calcium ionophores.

A review of insect stem cell types.

Insect stem cells have been described from both embryonic and adult tissues from a diversity of insect species, although much of the focus in insect stem cell research has been on Drosophila. Insects are a vast and diverse group and it is surprising that a critical aspect of their development like stem cells has not received more attention. In this review we discuss the current state of knowledge of insect stem cell types.

Microplitis demolitor bracovirus inhibits phagocytosis by hemocytes from Pseudoplusia includens.

The braconid wasp Microplitis demolitor carries Microplitis demolitor bracovirus (MdBV) and parasitizes the larval stage of several noctuid moths. A key function of MdBV in parasitism is suppression of the host's cellular immune response. Prior studies in the host Pseudoplusia includens indicated that MdBV blocks encapsulation by preventing two types of hemocytes, plasmatocytes and granulocytes, from adhering to foreign targets.