RAPD PCR Confirms Absence of Genetic Variation Between Insecticide Resistant Variants of the Green Peach Aphid, \u3ci\u3eMyzus Persicae\u3c/i\u3e (Homoptera: Aphididae)

Previous allozyme analysis has revealed an apparent absence of enzyme variability in the green peach aphid, Myzus persicae (Sulzer). We are interested in determining the genetic relatedness of individual M persicae clones carrying different numbers of esterase 4 (E4) gene copies conferring resistance to insecticides, in order to determine how many times and in what geographic locations resistance via gene duplication may have evolved. We have therefore extended the analysis of genetic variability in M. persicae to the DNA level using random amplification of polymorphic DNA (RAPD) with single 10 mer oligonucleotide primers. Here we report a lack of variability be- tween resistant clones in Wisconsin populations even at the DNA level Further, \u27fast\u27 E4 (FE4) variants appear to be absent from Wisconsin populations, despite FE4 variants of moderate resistance (Rl) being the most common clones in the United Kingdom. These results suggest that resistance in M. persicae may have evolved a very few times and that North American populations may differ from those in Europe by founder effects

Insecticide resistance comes of age

A new study integrates biochemistry, genetics and structural biology to reveal the mechanism of metabolic resistance in a vector mosquito in unprecedented detail

Butterfly gene flow goes berserk

This is the final version of the article. Available from the publisher via the DOI in this record.A new study shows that genomic introgression between two Heliconius butterfly species is not solely confined to color pattern loci.The authors work on butterfly wing patterning is supported by the BBSR

Sex, butterflies and molecular biology: when pigmentation met mimicry

No abstract is available for this article

Does resistance really carry a fitness cost?

This is the final version of the article. Available from Elsevier via the DOI in this record.Insecticide resistance mutations are widely assumed to carry fitness costs. However studies to measure such costs are rarely performed on genetically related strains and are often only done in the laboratory. Theory also suggests that once evolved the cost of resistance can be offset by the evolution of fitness modifiers. But for insecticide resistance only one such example is well documented. Here we critically examine the literature on fitness costs in the absence of pesticide and ask if our knowledge of molecular biology has helped us predict the costs associated with different resistance mechanisms. We find that resistance alleles can arise from pre-existing polymorphisms and resistance associated variation can also be maintained by sexual antagonism. We describe novel mechanisms whereby both resistant and susceptible alleles can be maintained in permanent heterozygosis and discuss the likely consequences for fitness both in the presence and absence of pesticide. Taken together these findings suggest that we cannot assume that resistance always appears de novo and that our assumptions about the associated fitness costs need to be informed by a deeper understanding of the underlying molecular biology.Work on insecticide resistance in the ffrench-Constant and Bass laboratories is supported by the BBSRC (BB/H014268 to R. ff-C), the Royal Society (Wolfson Merit Award to R. ff-C) and the ERC (ERC Consolidator award to CB)

Dynamic regulation of integrin activation by intracellular and extracellular signals controls oligodendrocyte morphology

RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are.Abstract Background Myelination requires precise control of oligodendrocyte morphology and myelin generation at each of the axons contacted by an individual cell. This control must involve the integration of extracellular cues, such as those on the axon surface, with intrinsic developmental programmes. We asked whether integrins represent one class of oligodendrocyte cell-surface receptors able to provide this integration. Results Integrins signal via a process of activation, a conformational change that can be induced either by "outside-in" signals comprising physiological extracellular matrix ligands (mimicked by the pharmacological use of the divalent cation manganese) or "inside-out" signalling molecules such as R-Ras. Increasing levels of outside-in signalling via the laminin receptor α6β1 integrin were found to promote oligodendrocyte processing and myelin sheet formation in culture. Similar results were obtained when inside-out signalling was increased by the expression of a constitutively-active R-Ras. Inhibiting inside-out signalling by using dominant-negative R-Ras reduces processes and myelin sheets; importantly, this can be partially rescued by the co-stimulation of outside-in signalling using manganese. Conclusion The balance of the equilibrium between active and inactive integrins regulates oligodendrocyte morphology, which is itself regulated by extrinsic and intrinsic cues so providing a mechanism of signal integration. As laminins capable of providing outside-in signals are present on axons at the time of myelination, a mechanism exists by which morphology and myelin generation might be regulated independently in each oligodendrocyte process.Peer Reviewe

Physical forces in myelination and repair: a question of balance?

A recent report in BMC Cell Biology examines how the balance of extracellular forces and intracellular contractions regulate the shape changes required for oligodendrocyte myelination. A failure of remyelination such as seen in multiple sclerosis could be caused by loss of this balance

Transposable elements and xenobiotic resistance

This is the final version. Available from Frontiers Media via the DOI in this record. Transposable elements or TEs are well known drivers of adaptive change in plants and animals but their role in insecticide resistance remains poorly documented. This review examines the potential role of transposons in resistance and identifies key areas where our understanding remains unclear. Despite well-known model systems such as upregulation of Drosophila Cyp6g1, many putative examples lack functional validation. The potential types of transposon-associated changes that could lead to resistance are reviewed, including changes in up-regulation, message stability, loss of function and alternative splicing. Where potential mechanisms appear absent from the resistance literature examples are drawn from other areas of biology. Finally, ways are suggested in which transgenic expression could be used to validate the biological significance of TE insertion. In the absence of such functional expression studies many examples of the association of TEs and resistance genes therefore remain as correlations.Biotechnology and Biological Sciences Research Council (BBSRC)European Research CouncilLeverhulme TrustRoyal Societ

The neural stem cell microenvironment

In mammals, neural stem cells appear early in development and remain active within the central nervous system for the whole life duration of the organism. During this developmental process they assume different cellular morphologies and reside within changing microenvironments whilst retaining the basic properties of a stem cell: multipotentiality and the ability to self renew. In this chapter, the basic morphological characteristics of neural stem cells will be reviewed, along with the fundamental structural components and signalling molecules of their microenvironments. In early neural development, when the patterning of the nervous system is established, neural stem cells are called neuroepithelial cells; they are situated among other neuroepithelial cells and they are exposed to various signals such as retinoic acid, sonic hedgehog and fibroblast growth factors. When neurogenesis commences, stem cells are transformed to radial glial cells and the complexity of their microenvironment increases due to the emergence of various types of neuronal progenitors, differentiated cells and extracellular signaling molecules. Finally, during adulthood, neural stem cells assume astroglial morphology and reside in specific microenvironments that are called neurogenic niches; small neurogenic islands where neurons and glia are continuously generated under the control of mechanisms largely similar to those operating during embryonic development

Hippocampal neurogenesis requires cell-autonomous thyroid hormone signaling

Adult hippocampal neurogenesis is strongly dependent on thyroid hormone (TH). Whether TH signaling regulates this process in a cell-autonomous or non-autonomous manner remains unknown. To answer this question, we used global and conditional knockouts of the TH transporter monocarboxylate transporter 8 (MCT8), having first used FACS and immunohistochemistry to demonstrate that MCT8 is the only TH transporter expressed on neuroblasts and adult slice cultures to confirm a necessary role for MCT8 in neurogenesis. Both mice with a global deletion or an adult neural stem cell-specific deletion of MCT8 showed decreased expression of the cell-cycle inhibitor P27KIP1, reduced differentiation of neuroblasts, and impaired generation of new granule cell neurons, with global knockout mice also showing enhanced neuroblast proliferation. Together, our results reveal a cell-autonomous role for TH signaling in adult hippocampal neurogenesis alongside non-cell-autonomous effects on cell proliferation earlier in the lineage