Emergence of cooperation and evolutionary stability in finite populations

To explain the evolution of cooperation by natural selection has been a major goal of biologists since Darwin. Cooperators help others at a cost to themselves, while defectors receive the benefits of altruism without providing any help in return. The standard game dynamical formulation is the 'Prisoner's Dilemma', in which two players have a choice between cooperation and defection. In the repeated game, cooperators using direct reciprocity cannot be exploited by defectors, but it is unclear how such cooperators can arise in the first place. In general, defectors are stable against invasion by cooperators. This understanding is based on traditional concepts of evolutionary stability and dynamics in infinite populations. Here we study evolutionary game dynamics in finite populations. We show that a single cooperator using a strategy like 'tit-for-tat' can invade a population of defectors with a probability that corresponds to a net selective advantage. We specify the conditions required for natural selection to favour the emergence of cooperation and define evolutionary stability in finite populations.     

A new intracellular medium for prolonged viability of noradrenergic storage vesicles from rat brain

Summary The biochemical lifetime of noradrenergic storage vesicles from rat brain is greatly extended in a medium based upon the membrane impermeable anion D-tartrate. Examination of the MgATP-dependent accumulation of (–)-³H-norepinephrine suggests that this medium may more closely approximate the intracellular environment of the storage vesicle, and may better support electrochemical gradients existing across the vesicle membrane.Acknowledgments. This work was supported by grant NS 15374 (NIH) of the United States Public Heath Service.     

Mantle compensation of active metamorphic core complexes at Woodlark rift in Papua New Guinea

In many highly extended rifts on the Earth, tectonic removal of the upper crust exhumes mid-crustal rocks, producing metamorphic core complexes. These structures allow the upper continental crust to accommodate tens of kilometres of extension, but it is not clear how the lower crust and underlying mantle respond. Also, despite removal of the upper crust, such core complexes remain both topographically high and in isostatic equilibrium. Because many core complexes in the western United States are underlain by a flat Moho discontinuity, it has been widely assumed that their elevation is supported by flow in the lower crust or by magmatic underplating. These processes should decouple upper-crust extension from that in the mantle. In contrast, here we present seismic observations of metamorphic core complexes of the western Woodlark rift that show the overall crust to be thinned beneath regions of greatest surface extension. These core complexes are actively being exhumed at a rate of 5-10 km Myr(-1), and the thinning of the underlying crust appears to be compensated by mantle rocks of anomalously low density, as indicated by low seismic velocities. We conclude that, at least in this case, the development of metamorphic core complexes and the accommodation of high extension is not purely a crustal phenomenon, but must involve mantle extension.     

Paxillin binds schwannomin and regulates its density-dependent localization and effect on cell morphology

Neurofibromatosis type 2 is an autosomal dominant disorder characterized by tumors, predominantly schwannomas, in the nervous system. It is caused by mutations in the gene NF2, encoding the growth regulator schwannomin (also known as merlin). Mutations occur throughout the 17-exon gene, with most resulting in protein truncation and undetectable amounts of schwannomin protein. Pathogenic mutations that result in production of defective schwannomin include in-frame deletions of exon 2 and three independent missense mutations within this same exon. Mice with conditional deletion of exon 2 in Schwann cells develop schwannomas, which confirms the crucial nature of exon 2 for growth control. Here we report that the molecular adaptor paxillin binds directly to schwannomin at residues 50-70, which are encoded by exon 2. This interaction mediates the membrane localization of schwannomin to the plasma membrane, where it associates with beta 1 integrin and erbB2. It defines a pathogenic mechanism for the development of NF2 in humans with mutations in exon 2 of NF2.     

Complete genome sequence of the model actinomycete Streptomyces coelicolor A3(2)

Streptomyces coelicolor is a representative of the group of soil-dwelling, filamentous bacteria responsible for producing most natural antibiotics used in human and veterinary medicine. Here we report the 8,667,507 base pair linear chromosome of this organism, containing the largest number of genes so far discovered in a bacterium. The 7,825 predicted genes include more than 20 clusters coding for known or predicted secondary metabolites. The genome contains an unprecedented proportion of regulatory genes, predominantly those likely to be involved in responses to external stimuli and stresses, and many duplicated gene sets that may represent 'tissue-specific' isoforms operating in different phases of colonial development, a unique situation for a bacterium. An ancient synteny was revealed between the central 'core' of the chromosome and the whole chromosome of pathogens Mycobacterium tuberculosis and Corynebacterium diphtheriae. The genome sequence will greatly increase our understanding of microbial life in the soil as well as aiding the generation of new drug candidates by genetic engineering.