Charge Transport in DNA-Based Devices

Charge migration along DNA molecules has attracted scientific interest for over half a century. Reports on possible high rates of charge transfer between donor and acceptor through the DNA, obtained in the last decade from solution chemistry experiments on large numbers of molecules, triggered a series of direct electrical transport measurements through DNA single molecules, bundles and networks. These measurements are reviewed and presented here. From these experiments we conclude that electrical transport is feasible in short DNA molecules, in bundles and networks, but blocked in long single molecules that are attached to surfaces. The experimental background is complemented by an account of the theoretical/computational schemes that are applied to study the electronic and transport properties of DNA-based nanowires. Examples of selected applications are given, to show the capabilities and limits of current theoretical approaches to accurately describe the wires, interpret the transport measurements, and predict suitable strategies to enhance the conductivity of DNA nanostructures.Comment: A single pdf file of 52 pages, containing the text and 23 figures. Review about direct measurements of DNA conductivity and related theoretical studies. For higher-resolution figures contact the authors or retrieve the original publications cited in the caption

Cellular localization of ERK in the R6/2 mouse model of Huntington’s disease

Introduction: The mitogen-activated protein kinases (MAPKs superfamily comprises three major signaling pathways: the extracellular signal- regulated protein kinases (ERKs), the c-Jun N-terminal kinases or stressactivated protein kinases (JNKs/ SAPKs) and the p38 family of kinases. ERK signaling has been implicated in a number of neurodegenerative disorders, including Huntington’s disease (HD). Phosphorylation patterns of ERK and JNK are altered in cell models of HD. In this study,we aimed at studying the correlations between ERK and the neuronal vulnerability to HD degeneration in the R6/2 transgenic mouse model of HD. Materials and methods: Immunohistochemistry for phospho-ERK (p-ERK, the activated form of ERK) and dual label immunofluorescence for p-ERK and each of the striatal neuronalmarkers were employed on perfusion-fixed brain sections from R6/2 and wildtype mice. Results: Our study shows that striatal neurons, both spiny projection and interneurons, are completely devoid of p-ERK immunoreactivity in the wild-type mouse.Conversely, parvalbumin- labeled GABAergic interneurons of the striatum are highly enriched in p-ERK in the R6/2 mice, cholinergic and somatostatinergic interneurons are devoid of it. Interestingly, the parvalbuminergic interneuron subpopulation of the striatum is the only interneuron subset that is extremely prone to degenerate in HD. Conclusions: Thus, our study confirms and extends the concept that the expression of phosphorilated ERK is related to neuronal vulnerability and is implicated in the pathophysiology of cell death in HD