Understanding and tuning the epitaxy of large aromatic adsorbates by molecular design

If the rich functionality of organic molecules is to be exploited in devices such as light-emitting diodes or field-effect transistors, interface properties of organic materials with various (metallic and insulating) substrates must be tailored carefully. In many cases, this calls for well-ordered interfaces. Organic epitaxy-that is, the growth of molecular films with a commensurate structural relationship to their crystalline substrates--relies on successful recognition of preferred epitaxial sites. For some large pi-conjugated molecules ('molecular platelets') this works surprisingly well, even if the substrate exhibits no template structure into which the molecules can lock. Here we present an explanation for site recognition in non-templated organic epitaxy, and thus resolve a long-standing puzzle. We propose that this form of site recognition relies on the existence of a local molecular reaction centre in the extended pi-electron system of the molecule. Its activity can be controlled by appropriate side groups and--in a certain regime--may also be probed by molecularly sensitized scanning tunnelling microscopy. Our results open the possibility of engineering epitaxial interfaces, as well as other interfacial nanostructures for which specific site recognition is essential.     

The microRNA-producing enzyme Dicer1 is essential for zebrafish development

MicroRNAs (miRNAs) are produced by the Dicer1 enzyme; the role of Dicer1 in vertebrate development is unknown. Here we report target-selected inactivation of the dicer1 gene in zebrafish. We observed an initial build-up of miRNA levels, produced by maternal Dicer1, in homozygous dicer1 mutants, but miRNA accumulation stopped after a few days. This resulted in developmental arrest around day 10. These results indicate that miRNA-producing Dicer1 is essential for vertebrate development.     

Interaction of reelin signaling and Lis1 in brain development

Loss-of-function mutations in RELN (encoding reelin) or PAFAH1B1 (encoding LIS1) cause lissencephaly, a human neuronal migration disorder. In the mouse, homozygous mutations in Reln result in the reeler phenotype, characterized by ataxia and disrupted cortical layers. Pafah1b1(+/-) mice have hippocampal layering defects, whereas homozygous mutants are embryonic lethal. Reln encodes an extracellular protein that regulates layer formation by interacting with VLDLR and ApoER2 (Lrp8) receptors, thereby phosphorylating the Dab1 signaling molecule. Lis1 associates with microtubules and modulates neuronal migration. We investigated interactions between the reelin signaling pathway and Lis1 in brain development. Compound mutant mice with disruptions in the Reln pathway and heterozygous Pafah1b1 mutations had a higher incidence of hydrocephalus and enhanced cortical and hippocampal layering defects. Dab1 and Lis1 bound in a reelin-induced phosphorylation-dependent manner. These data indicate genetic and biochemical interaction between the reelin signaling pathway and Lis1.