Surface transfer doping of diamond

The electronic properties of many materials can be controlled by introducing appropriate impurities into the bulk crystal lattice in a process known as doping. In this way, diamond (a well-known insulator) can be transformed into a semiconductor, and recent progress in thin-film diamond synthesis has sparked interest in the potential applications of semiconducting diamond. However, the high dopant activation energies (in excess of 0.36 eV) and the limitation of donor incorporation to (111) growth facets only have hampered the development of diamond-based devices. Here we report a doping mechanism for diamond, using a method that does not require the introduction of foreign atoms into the diamond lattice. Instead, C60 molecules are evaporated onto the hydrogen-terminated diamond surface, where they induce a subsurface hole accumulation and a significant rise in two-dimensional conductivity. Our observations bear a resemblance to the so-called surface conductivity of diamond seen when hydrogenated diamond surfaces are exposed to air, and support an electrochemical model in which the reduction of hydrated protons in an aqueous surface layer gives rise to a hole accumulation layer. We expect that transfer doping by C60 will open a broad vista of possible semiconductor applications for diamond.     

Palaeobiology: Argentinian unhatched pterosaur fossil

Our knowledge of the eggs and embryos of pterosaurs, the Mesozoic flying reptiles, is sparse. Until now, the recent discovery of an ornithocheirid embryo from 121-million-year-old rocks in China constituted the only reliable evidence of an unhatched pterosaur. Here we describe an embryonic fossil of a different pterosaur from the Early Cretaceous lacustrine deposits of Loma del Pterodaustro (the Lagarcito Formation, which is about 100 million years old) in central Argentina. This new fossil provides insight into the eggshell morphology, early growth and nesting environments of pterosaurs.     

Origin of AIDS: contaminated polio vaccine theory refuted

Despite strong evidence to the contrary, speculation continues that the AIDS virus, human immunodeficiency virus type 1 (HIV-1), may have crossed into humans as a result of contamination of the oral polio vaccine (OPV). This 'OPV/AIDS theory' claims that chimpanzees from the vicinity of Stanleyville--now Kisangani in the Democratic Republic of Congo--were the source of a simian immunodeficiency virus (SIVcpz) that was transmitted to humans when chimpanzee tissues were allegedly used in the preparation of OPV. Here we show that SIVcpz is indeed endemic in wild chimpanzees of this region but that the circulating virus is phylogenetically distinct from all strains of HIV-1, providing direct evidence that these chimpanzees were not the source of the human AIDS pandemic.     

Pilus chaperones represent a new type of protein-folding catalyst

Adhesive type 1 pili from uropathogenic Escherichia coli strains have a crucial role during infection by mediating the attachment to and potentially the invasion of host tissue. These filamentous, highly oligomeric protein complexes are assembled by the 'chaperone-usher' pathway, in which the individual pilus subunits fold in the bacterial periplasm and form stoichiometric complexes with a periplasmic chaperone molecule that is essential for pilus assembly. The chaperone subsequently delivers the subunits to an assembly platform (usher) in the outer membrane, which mediates subunit assembly and translocation to the cell surface. Here we show that the periplasmic type 1 pilus chaperone FimC binds non-native pilus subunits and accelerates folding of the subunit FimG by 100-fold. Moreover, we find that the FimC-FimG complex is formed quantitatively and very rapidly when folding of FimG is initiated in the presence of both FimC and the assembly-competent subunit FimF, even though the FimC-FimG complex is thermodynamically less stable than the FimF-FimG complex. FimC thus represents a previously unknown type of protein-folding catalyst, and simultaneously acts as a kinetic trap preventing spontaneous subunit assembly in the periplasm.