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In the last years coating of surfaces in the presence of dopamine or other catecholamines in oxidative conditions to yield "polydopamine" films has become a popular, easy and versatile coating methodology. Polydopamine(s) offer(s) also a rich chemistry allowing to post-functionalize the obtained coatings with metal nanoparticles with polymers and proteins. However, the interactions either of covalent or non-covalent nature between polydopamine and biomolecules has only been explored more recently. They allow polydopamine to become a material, in the form of nanoparticles, membranes and other assemblies, in its own right not just as a coating. It is the aim of this review to describe the most recent advances in the design of composites between polydopamine and related eumelanin like materials with biomolecules like proteins, nucleotides, oligosaccharides and lipid assemblies. Furthermore, the interactions between polydopamine and living cells will be also reported.

© 2017 American Chemical Society.The design and use of materials in the nanoscale size range for addressing medical and health-related issues continues to receive increasing interest. Research in nanomedicine spans a multitude of areas, including drug delivery, vaccine development, antibacterial, diagnosis and imaging tools, wearable devices, implants, high-throughput screening platforms, etc. using biological, nonbiological, biomimetic, or hybrid materials. Many of these developments are starting to be translated into viable clinical products. Here, we provide an overview of recent developments in nanomedicine and highlight the current challenges and upcoming opportunities for the field and translation to the clinic.

Funder: German Research Foundation; Id: http://dx.doi.org/10.13039/501100001659, Amyloid‐like peptide nanofibrils (PNFs) are abundant in nature providing rich bioactivities and playing both functional and pathological roles. The structural features responsible for their unique bioactivities are, however, still elusive. Supramolecular nanostructures are notoriously challenging to optimize, as sequence changes affect self‐assembly, fibril morphologies, and biorecognition. Herein, the first sequence optimization of PNFs, derived from the peptide enhancing factor‐C (EF‐C, QCKIKQIINMWQ), for enhanced retroviral gene transduction via a multiparameter and a multiscale approach is reported. Retroviral gene transfer is the method of choice for the stable delivery of genetic information into cells offering great perspectives for the treatment of genetic disorders. Single fibril imaging, zeta potential, vibrational spectroscopy, and quantitative retroviral transduction assays provide the structure parameters responsible for PNF assembly, fibrils morphology, secondary and quaternary structure, and PNF‐virus‐cell interactions. Optimized peptide sequences such as the 7‐mer, CKFKFQF, have been obtained quantitatively forming supramolecular nanofibrils with high intermolecular β‐sheet content that efficiently bind virions and attach to cellular membranes revealing efficient retroviral gene transfer.

mRNA localisation and translational control is a conserved, universal process involved in a number of essential cellular processes. Localised mRNAs are processed throughout their life cycle from transcription to degradation. How and where key mRNA remodelling steps occur is unclear. Furthermore, how mRNAs are translationally repressed during their transport, but translationally activated once localised, is a key question in the field. The Drosophila oocyte is a well used model system, and is patterned by the differential localisation of gurken, bicoid, oskar and nanos, which are all transcribed in the nuclei of the adjacent supporting nurse cell tissue. Here, I image localised mRNAs in live nurse cells and detect gurken with single molecule fluorescent in-situ hybridisation techniques for the first time. I use these assays to characterise the properties of gurken and oskar mRNAs in the nurse cells, and show they are strikingly different to the oocyte. I find that Processing bodies, which are key sites of translational regulation in the oocyte, contain significantly lower levels of the translational activator and Drosophila CPEB homolog, Orb. I show that, in contrast to oskar, whose translation is prevented during transport mainly by repressor proteins, gurken mRNA translation in the nurse cells is not prevented by a single repressor, but rather the absence of its translational activator, Orb/CPEB, in this tissue. Ectopic expression of Orb in the nurse cells is sufficient for the association of gurken with Processing bodies and premature gurken translation. These data highlight a new model for translational regulation through restricted spatial access to a translational activator, and I propose that such a mechanism could be widely deployed in other tissues.