Host sanctions and the legume-rhizobium mutualism

Explaining mutualistic cooperation between species remains one of the greatest problems for evolutionary biology. Why do symbionts provide costly services to a host, indirectly benefiting competitors sharing the same individual host? Host monitoring of symbiont performance and the imposition of sanctions on 'cheats' could stabilize mutualism. Here we show that soybeans penalize rhizobia that fail to fix N(2) inside their root nodules. We prevented a normally mutualistic rhizobium strain from cooperating (fixing N(2)) by replacing air with an N(2)-free atmosphere (Ar:O(2)). A series of experiments at three spatial scales (whole plants, half root systems and individual nodules) demonstrated that forcing non-cooperation (analogous to cheating) decreased the reproductive success of rhizobia by about 50%. Non-invasive monitoring implicated decreased O(2) supply as a possible mechanism for sanctions against cheating rhizobia. More generally, such sanctions by one or both partners may be important in stabilizing a wide range of mutualistic symbioses.     

Cooperation and conflict in quorum-sensing bacterial populations

It has been suggested that bacterial cells communicate by releasing and sensing small diffusible signal molecules in a process commonly known as quorum sensing (QS). It is generally assumed that QS is used to coordinate cooperative behaviours at the population level. However, evolutionary theory predicts that individuals who communicate and cooperate can be exploited. Here we examine the social evolution of QS experimentally in the opportunistic pathogen Pseudomonas aeruginosa, and show that although QS can provide a benefit at the group level, exploitative individuals can avoid the cost of producing the QS signal or of performing the cooperative behaviour that is coordinated by QS, and can therefore spread. We also show that a solution to the problem of exploitation is kin selection, if interacting bacterial cells tend to be close relatives. These results show that the problem of exploitation, which has been the focus of considerable attention in animal communication, also arises in bacteria.     

Atomic structures of amyloid cross-beta spines reveal varied steric zippers

Amyloid fibrils formed from different proteins, each associated with a particular disease, contain a common cross-beta spine. The atomic architecture of a spine, from the fibril-forming segment GNNQQNY of the yeast prion protein Sup35, was recently revealed by X-ray microcrystallography. It is a pair of beta-sheets, with the facing side chains of the two sheets interdigitated in a dry 'steric zipper'. Here we report some 30 other segments from fibril-forming proteins that form amyloid-like fibrils, microcrystals, or usually both. These include segments from the Alzheimer's amyloid-beta and tau proteins, the PrP prion protein, insulin, islet amyloid polypeptide (IAPP), lysozyme, myoglobin, alpha-synuclein and beta(2)-microglobulin, suggesting that common structural features are shared by amyloid diseases at the molecular level. Structures of 13 of these microcrystals all reveal steric zippers, but with variations that expand the range of atomic architectures for amyloid-like fibrils and offer an atomic-level hypothesis for the basis of prion strains.     

The role of fluids in lower-crustal earthquakes near continental rifts

The occurrence of earthquakes in the lower crust near continental rifts has long been puzzling, as the lower crust is generally thought to be too hot for brittle failure to occur. Such anomalous events have usually been explained in terms of the lower crust being cooler than normal. But if the lower crust is indeed cold enough to produce earthquakes, then the uppermost mantle beneath it should also be cold enough, and yet uppermost mantle earthquakes are not observed. Numerous lower-crustal earthquakes occur near the southwestern termination of the Taupo Volcanic Zone (TVZ), an active continental rift in New Zealand. Here we present three-dimensional tomographic imaging of seismic velocities and seismic attenuation in this region using data from a dense seismograph deployment. We find that crustal earthquakes accurately relocated with our three-dimensional seismic velocity model form a continuous band along the rift, deepening from mostly less than 10 km in the central TVZ to depths of 30-40 km in the lower crust, 30 km southwest of the termination of the volcanic zone. These earthquakes often occur in swarms, suggesting fluid movement in critically loaded fault zones. Seismic velocities within the band are also consistent with the presence of fluids, and the deepening seismicity parallels the boundary between high seismic attenuation (interpreted as partial melt) within the central TVZ and low seismic attenuation in the crust to the southwest. This linking of upper and lower-crustal seismicity and crustal structure allows us to propose a common explanation for all the seismicity, involving the weakening of faults on the periphery of an otherwise dry, mafic crust by hot fluids, including those exsolved from underlying melt. Such fluids may generally be an important driver of lower-crustal seismicity near continental rifts.     

Dnmt3a silences hematopoietic stem cell self-renewal

DNA methylation is an epigenetic mark stably directing gene expression throughout development. A new study uncovers a role for the DNA methyltransferase Dnmt3a in silencing self-renewal genes in hematopoietic stem cells (HSCs) to permit efficient hematopoietic differentiation.     

<Emphasis Type="Italic">O</Emphasis>-Mannosylation and human disease

Glycosylation of proteins is arguably the most prevalent co- and post-translational modification. It is responsible for increased heterogeneity and functional diversity of proteins. Here we discuss the importance of one type of glycosylation, specifically O-mannosylation and its relationship to a number of human diseases. The most widely studied O-mannose modified protein is alpha-dystroglycan (α-DG). Recent studies have focused intensely on α-DG due to the severity of diseases associated with its improper glycosylation. O-mannosylation of α-DG is involved in cancer metastasis, arenavirus entry, and multiple forms of congenital muscular dystrophy [1, 2]. In this review, we discuss the structural and functional characteristics of O-mannose-initiated glycan structures on α-DG, enzymes involved in the O-mannosylation pathway, and the diseases that are a direct result of disruptions within this pathway.