Facultative cheater mutants reveal the genetic complexity of cooperation in social amoebae

Cooperation is central to many major transitions in evolution, including the emergence of eukaryotic cells, multicellularity and eusociality. Cooperation can be destroyed by the spread of cheater mutants that do not cooperate but gain the benefits of cooperation from others. However, cooperation can be preserved if cheaters are facultative, cheating others but cooperating among themselves. Several cheater mutants have been studied before, but no study has attempted a genome-scale investigation of the genetic opportunities for cheating. Here we describe such a screen in a social amoeba and show that cheating is multifaceted by revealing cheater mutations in well over 100 genes of diverse types. Many of these mutants cheat facultatively, producing more than their fair share of spores in chimaeras, but cooperating normally when clonal. These findings indicate that phenotypically stable cooperative systems may nevertheless harbour genetic conflicts. The opportunities for evolutionary moves and countermoves in such conflicts may select for the involvement of multiple pathways and numerous genes.     

A theoretical look at the direct detection of giant planets outside the Solar System

Astronomy is at times a science of unexpected discovery. When it is, and if we are lucky, new intellectual territories emerge to challenge our views of the cosmos. The recent indirect detections using high-precision Doppler spectroscopy of more than 100 giant planets orbiting more than 100 nearby stars is an example of such rare serendipity. What has been learned has shaken out preconceptions, for none of the planetary systems discovered so far is like our own. The key to unlocking a planet's chemical, structural, and evolutionary secrets, however, is the direct detection of the planet's light. Because there have been as yet no confirmed detections, a theoretical analysis of such a planet's atmosphere is necessary for guiding our search.     

Epistasis analysis with global transcriptional phenotypes

Classical epistasis analysis can determine the order of function of genes in pathways using morphological, biochemical and other phenotypes. It requires knowledge of the pathway's phenotypic output and a variety of experimental expertise and so is unsuitable for genome-scale analysis. Here we used microarray profiles of mutants as phenotypes for epistasis analysis. Considering genes that regulate activity of protein kinase A in Dictyostelium, we identified known and unknown epistatic relationships and reconstructed a genetic network with microarray phenotypes alone. This work shows that microarray data can provide a uniform, quantitative tool for large-scale genetic network analysis.     

Seasonal prediction of hurricane activity reaching the coast of the United States

Much of the property damage from natural hazards in the United States is caused by landfalling hurricanes--strong tropical cyclones that reach the coast. For the southeastern Atlantic coast of the US, a statistical method for forecasting the occurrence of landfalling hurricanes for the season ahead has been reported, but the physical mechanisms linking the predictor variables to the frequency of hurricanes remain unclear. Here we present a statistical model that uses July wind anomalies between 1950 and 2003 to predict with significant and useful skill the wind energy of US landfalling hurricanes for the following main hurricane season (August to October). We have identified six regions over North America and over the east Pacific and North Atlantic oceans where July wind anomalies, averaged between heights of 925 and 400 mbar, exhibit a stationary and significant link to the energy of landfalling hurricanes during the subsequent hurricane season. The wind anomalies in these regions are indicative of atmospheric circulation patterns that either favour or hinder evolving hurricanes from reaching US shores.     

Positron emission tomography after MPTP: observations relating to the cause of Parkinson's disease

The dopa analogue 6-fluorodopa (6-FD) used with positron emission tomography (PET) allows in vivo visualization of dopamine and its metabolites in nigrostriatal nerve endings. We have now found abnormal 6-FD scans in four subjects exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). None had parkinsonism. The results suggest subclinical damage to the nigrostriatal pathway. This is the first direct evidence that dopaminergic impairment can exist without clinical deficits. Here we discuss this finding in the context of the hypothesis that Parkinson's disease may stem from clinically silent damage to the substantia nigra, followed by slow attrition of neurones in this region because of its particular vulnerability to cell loss as a normal consequence of ageing.     

Osmotic Pressure of Water in Nafion~

Mechanical failure modes leading to cracks or breeches in proton exchange membrane fuel cells are driven by mechanical forces associated with swelling from water uptake and shrinkage from dehumidifi-cation. To determine the magnitude of compressive mechanical stress imposed by water swelling in a proton exchange fuel-cell membrane, the osmotic pressure of water in a perfluorosulfonic acid ionomer (Nafion? N 117) membrane was measured using a hydrostatic piston-cylinder device with an in-situ hydrophilic frit. Experiments indicate that hydrostatic stresses greater than 103.5 MPa are created in a membrane when swollen with water at 23℃ suggesting that pressure from water swelling can distort Nafion N 117-based structures as the osmotic pressure is of the same order of magnitude as the flow stress of Nafion N 117.     

Regulation of angiogenesis by a non-canonical Wnt-Flt1 pathway in myeloid cells

Myeloid cells are a feature of most tissues. Here we show that during development, retinal myeloid cells (RMCs) produce Wnt ligands to regulate blood vessel branching. In the mouse retina, where angiogenesis occurs postnatally, somatic deletion in RMCs of the Wnt ligand transporter Wntless results in increased angiogenesis in the deeper layers. We also show that mutation of Wnt5a and Wnt11 results in increased angiogenesis and that these ligands elicit RMC responses via a non-canonical Wnt pathway. Using cultured myeloid-like cells and RMC somatic deletion of Flt1, we show that an effector of Wnt-dependent suppression of angiogenesis by RMCs is Flt1, a naturally occurring inhibitor of vascular endothelial growth factor (VEGF). These findings indicate that resident myeloid cells can use a non-canonical, Wnt-Flt1 pathway to suppress angiogenic branching.