Maize yellow stripe1 encodes a membrane protein directly involved in Fe(III) uptake

Frequently, crop plants do not take up adequate amounts of iron from the soil, leading to chlorosis, poor yield and decreased nutritional quality. Extremely limited soil bioavailability of iron has led plants to evolve two distinct uptake strategies: chelation, which is used by the world's principal grain crops; and reduction, which is used by other plant groups. The chelation strategy involves extrusion of low-molecular-mass secondary amino acids (mugineic acids) known as 'phytosiderophores' which chelate sparingly soluble iron. The Fe(III)-phytosiderophore complex is then taken up by an unknown transporter at the root surface. The maize yellow stripe1 (ys1) mutant is deficient in Fe(III)-phytosiderophore uptake, therefore YS1 has been suggested to be the Fe(III)-phytosiderophore transporter. Here we show that ys1 is a membrane protein that mediates iron uptake. Expression of YS1 in a yeast iron uptake mutant restores growth specifically on Fe(III)-phytosiderophore media. Under iron-deficient conditions, ys1 messenger RNA levels increase in both roots and shoots. Cloning of ys1 is an important step in understanding iron uptake in grasses, and has implications for mechanisms controlling iron homeostasis in all plants.     

Wolbachia-induced incompatibility precedes other hybrid incompatibilities in Nasonia

Wolbachia are cytoplasmically inherited bacteria that cause a number of reproductive alterations in insects, including cytoplasmic incompatibility, an incompatibility between sperm and egg that results in loss of sperm chromosomes following fertilization. Wolbachia are estimated to infect 15-20% of all insect species, and also are common in arachnids, isopods and nematodes. Therefore, Wolbachia-induced cytoplasmic incompatibility could be an important factor promoting rapid speciation in invertebrates, although this contention is controversial. Here we show that high levels of bidirectional cytoplasmic incompatibility between two closely related species of insects (the parasitic wasps Nasonia giraulti and Nasonia longicornis) preceded the evolution of other postmating reproductive barriers. The presence of Wolbachia severely reduces the frequency of hybrid offspring in interspecies crosses. However, antibiotic curing of the insects results in production of hybrids. Furthermore, F1 and F2 hybrids are completely viable and fertile, indicating the absence of F1 and F2 hybrid breakdown. Partial interspecific sexual isolation occurs, yet it is asymmetric and incomplete. Our results indicate that Wolbachia-induced reproductive isolation occurred in the early stages of speciation in this system, before the evolution of other postmating isolating mechanisms (for example, hybrid inviability and hybrid sterility).     

Hemispherical variations in seismic velocity at the top of the Earth's inner core

Knowledge of the seismic velocity structure at the top of the Earth's inner core is important for deciphering the physical processes responsible for inner-core growth. Previous global seismic studies have focused on structures found 100 km or deeper within the inner core, with results for the uppermost 100 km available for only isolated regions. Here we present constraints on seismic velocity variations just beneath the inner-core boundary, determined from the difference in travel time between waves reflected at the inner-core boundary and those transmitted through the inner core. We found that these travel-time residuals-observed on both global seismograph stations and several regional seismic networks-are systematically larger, by about 0.8 s, for waves that sample the 'eastern hemisphere' of the inner core (40 degrees E to 180 degrees E) compared to those that sample the 'western hemisphere' (180 degrees W to 40 degrees E). These residuals show no correlation with the angle at which the waves traverse the inner core; this indicates that seismic anisotropy is not strong in this region and that the isotropic seismic velocity of the eastern hemisphere is about 0.8% higher than that of the western hemisphere.     

Linkage disequilibrium in the human genome

With the availability of a dense genome-wide map of single nucleotide polymorphisms (SNPs), a central issue in human genetics is whether it is now possible to use linkage disequilibrium (LD) to map genes that cause disease. LD refers to correlations among neighbouring alleles, reflecting 'haplotypes' descended from single, ancestral chromosomes. The size of LD blocks has been the subject of considerable debate. Computer simulations and empirical data have suggested that LD extends only a few kilobases (kb) around common SNPs, whereas other data have suggested that it can extend much further, in some cases greater than 100 kb. It has been difficult to obtain a systematic picture of LD because past studies have been based on only a few (1-3) loci and different populations. Here, we report a large-scale experiment using a uniform protocol to examine 19 randomly selected genomic regions. LD in a United States population of north-European descent typically extends 60 kb from common alleles, implying that LD mapping is likely to be practical in this population. By contrast, LD in a Nigerian population extends markedly less far. The results illuminate human history, suggesting that LD in northern Europeans is shaped by a marked demographic event about 27,000-53,000 years ago.     

ICOS is essential for effective T-helper-cell responses

The outcome of T-cell responses after T-cell encounter with specific antigens is modulated by co-stimulatory signals, which are required for both lymphocyte activation and development of adaptive immunity. ICOS, an inducible co-stimulator with homology to CD28, is expressed on activated, but not resting T cells, and shows T-cell co-stimulatory function in vitro. ICOS binds specifically to its counter-receptor B7RP-1 (refs 5,6,7), but not to B7-1 or B7-2. Here we provide in vivo genetic evidence that ICOS delivers a co-stimulatory signal that is essential both for efficient interaction between T and B cells and for normal antibody responses to T-cell-dependent antigens. To determine the physiological function of ICOS, we generated and characterized gene-targeted ICOS-deficient mice. In vivo, a lack of ICOS results in severely deficient T-cell-dependent B-cell responses. Germinal centre formation is impaired and immunoglobulin class switching, including production of allergy-mediating IgE, is defective. ICOS-deficient T cells primed in in vivo and restimulated in vitro with specific antigen produce only low levels of interleukin-4, but remain fully competent to produce interferon-gamma.     

A high-velocity black hole on a Galactic-halo orbit in the solar neighbourhood

Only a few of the dozen or so known stellar-mass black holes have been observed away from the plane of the Galaxy. Those few could have been ejected from the plane as a result of a 'kick' received during a supernova explosion, or they could be remnants of the population of massive stars formed in the early stages of evolution of the Galaxy. Determining their orbital motion should help to distinguish between these options. Here we report the transverse motion (in the plane of the sky) for the black-hole X-ray nova XTE J1118+480 (refs 2, 3, 4, 5), from which we derive a large space velocity. This X-ray binary system has an eccentric orbit around the Galactic Centre, like most objects in the halo of the Galaxy, such as ancient stars and globular clusters. The properties of the system suggest that its age is comparable to or greater than the age of the Galactic disk. Only an extraordinary 'kick' from a supernova could have launched the black hole into an orbit like this from a birthplace in the disk of the Galaxy.     

The RNA component of telomerase is mutated in autosomal dominant dyskeratosis congenita

Dyskeratosis congenita is a progressive bone-marrow failure syndrome that is characterized by abnormal skin pigmentation, leukoplakia and nail dystrophy. X-linked, autosomal recessive and autosomal dominant inheritance have been found in different pedigrees. The X-linked form of the disease is due to mutations in the gene DKC1 in band 2, sub-band 8 of the long arm of the X chromosome (ref. 3). The affected protein, dyskerin, is a nucleolar protein that is found associated with the H/ACA class of small nucleolar RNAs and is involved in pseudo-uridylation of specific residues of ribosomal RNA. Dyskerin is also associated with telomerase RNA (hTR), which contains a H/ACA consensus sequence. Here we map the gene responsible for dyskeratosis congenita in a large pedigree with autosomal dominant inheritance. Affected members of this family have an 821-base-pair deletion on chromosome 3q that removes the 3' 74 bases of hTR. Mutations in hTR were found in two other families with autosomal dominant dyskeratosis congenita.     

The physical maps for sequencing human chromosomes 1, 6, 9, 10, 13, 20 and X

We constructed maps for eight chromosomes (1, 6, 9, 10, 13, 20, X and (previously) 22), representing one-third of the genome, by building landmark maps, isolating bacterial clones and assembling contigs. By this approach, we could establish the long-range organization of the maps early in the project, and all contig extension, gap closure and problem-solving was simplified by containment within local regions. The maps currently represent more than 94% of the euchromatic (gene-containing) regions of these chromosomes in 176 contigs, and contain 96% of the chromosome-specific markers in the human gene map. By measuring the remaining gaps, we can assess chromosome length and coverage in sequenced clones.