Reproductive isolation caused by colour pattern mimicry

Speciation is facilitated if ecological adaptation directly causes assortative mating, but few natural examples are known. Here we show that a shift in colour pattern mimicry was crucial in the origin of two butterfly species. The sister species Heliconius melpomene and Heliconius cydno recently diverged to mimic different model taxa, and our experiments show that their mimetic coloration is also important in choosing mates. Assortative mating between the sister species means that hybridization is rare in nature, and the few hybrids that are produced are non-mimetic, poorly adapted intermediates. Thus, the mimetic shift has caused both pre-mating and post-mating isolation. In addition, individuals from a population of H. melpomene allopatric to H. cydno court and mate with H. cydno more readily than those from a sympatric population. This suggests that assortative mating has been enhanced in sympatry.     

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.     

An auroral flare at Jupiter

Jupiter's aurora is the most powerful in the Solar System. It is powered largely by energy extracted from planetary rotation, although there seems also to be a contribution from the solar wind. This contrasts with Earth's aurora, which is generated through the interaction of the solar wind with the magnetosphere. The major features of Jupiter's aurora (based on far-ultraviolet, near-infrared and visible-wavelength observations) include a main oval that generally corotates with the planet and a region of patchy, diffuse emission inside the oval on Jupiter's dusk side. Here we report the discovery of a rapidly evolving, very bright and localized emission poleward of the northern main oval, in a region connected magnetically to Jupiter's outer magnetosphere. The intensity of the emission increased by a factor of 30 within 70 s, and then decreased on a similar timescale, all captured during a single four-minute exposure. This type of flaring emission has not previously been reported for Jupiter (similar, but smaller, transient events have been observed at Earth), and it may be related directly to changes in the solar wind.     

A massive reservoir of low-excitation molecular gas at high redshift

Molecular hydrogen (H2) is an important component of galaxies because it fuels star formation and the accretion of gas onto active galactic nuclei (AGN), the two processes that can generate the large infrared luminosities of gas-rich galaxies. Observations of spectral-line emission from the tracer molecule carbon monoxide (CO) are used to probe the properties of this gas. But the lines that have been studied in the local Universe-mostly the lower rotational transitions of J = 1 --> 0 and J = 2 --> 1-have hitherto been unobservable in high-redshift galaxies. Instead, higher transitions have been used, although the densities and temperatures required to excite these higher transitions may not be reached by much of the gas. As a result, past observations may have underestimated the total amount of molecular gas by a substantial amount. Here we report the discovery of large amounts of low-excitation molecular gas around the infrared-luminous quasar APM08279+5255 at redshift z = 3.91, using the two lowest excitation lines of 12 CO (J = 1 --> 0 and J = 2 --> 1). The maps confirm the presence of hot and dense gas near the nucleus, and reveal an extended reservoir of molecular gas with low excitation that is 10 to 100 times more massive than the gas traced by the higher-excitation observations. This raises the possibility that significant amounts of low-excitation molecular gas may exist in the environments of high-redshift (z > 3) galaxies.     

An agrin minigene rescues dystrophic symptoms in a mouse model for congenital muscular dystrophy

Congenital muscular dystrophy is a heterogeneous and severe, progressive muscle-wasting disease that frequently leads to death in early childhood. Most cases of congenital muscular dystrophy are caused by mutations in LAMA2, the gene encoding the alpha2 chain of the main laminin isoforms expressed by muscle fibres. Muscle fibre deterioration in this disease is thought to be caused by the failure to form the primary laminin scaffold, which is necessary for basement membrane structure, and the missing interaction between muscle basement membrane and the dystrophin-glycoprotein complex (DGC) or the integrins. With the aim to restore muscle function in a mouse model for this disease, we have designed a minigene of agrin, a protein known for its role in the formation of the neuromuscular junction. Here we show that this mini-agrin-which binds to basement membrane and to alpha-dystroglycan, a member of the DGC-amends muscle pathology by a mechanism that includes agrin-mediated stabilization of alpha-dystroglycan and the laminin alpha5 chain. Our data provides in vivo evidence that a non-homologous protein in combination with rational protein design can be used to devise therapeutic tools that may restore muscle function in human muscular dystrophies.