In This Issue
GEOPHYSICS
Global heat flow fluctuates more than previously thought
Like an oven, office building, or the human body, the Earth loses heat produced in its interior via diffusion through its surface. Approximately 70% of the Earth's heat loss flows through the oceanic lithosphere (the crust and uppermost mantle), principally through young, hot crust that erupts to the surface during the formation of mountainous oceanic ridges. Taking advantage of recent reconstructions of seafloor age, Sean Loyd et al. modeled the trends in the Earth's oceanic heat flow over the last 65 million years. They found that, even though the amount of seafloor has increased by 8% during this time, heat flow has been decreasing by 0.15% every million years, an order of magnitude faster than typical estimates of cooling trends. This rapid decrease may be indicative of fluctuations in the way plate tectonics works over time. The cause for this shrinking heat flow, Loyd et al. say, is a decrease in the surface area of young, ridge-proximal crust due to the merging of oceanic plates in the Pacific basin. The authors also note that these findings provide evidence of how continents and oceanic plates self-organize to transport heat. — N.Z.
“Time variability in Cenozoic reconstructions of mantle heat flow: Plate tectonic cycles and implications for Earth's thermal evolution” by S. J. Loyd, T. W. Becker, C. P. Conrad, C. Lithgow-Bertelloni, and F. A. Corsetti (see pages 14266–14271)
APPLIED BIOLOGICAL SCIENCES, ENGINEERING
Modular riboswitches
Natural riboswitches control gene expression in bacteria and eukaryotes. In a synthetic riboswitch engineered by Maung Win and Christina Smolke, an aptamer, which binds a small-molecule ligand, is coupled to a ribozyme. Upon ligand binding, aptamer conformational change is transmitted to the ribozyme, which turns mRNA translation on or off. The authors developed the concept of modular riboswitch design for bioengineering. They report prototypes in which custom ribo switches function either as sensors or growth triggers. Their model is the “hammerhead ribozyme,” a T-shaped molecule joined to an mRNA by its stem. At the end of the T arms are two loops whose integrity is essential for ribozyme function: self-cleavage, which renders the mRNA nonfunctional. The authors integrate an aptamer into one of the T-arm loops; on shifting conformation, the aptamer disrupts the ribozyme structure and turns it off. (Alternatively, ligand binding can restore ribozyme structure to turn it on.) The riboswitches function in vivo, inserted within plasmids into Saccharomyces cerevisiae, with aptamers sensitive to either theophylline or tetracycline. The aptamer role could, in theory, be played by any of a wide range of RNA sequences that bind small molecules. — K.M.
“A modular and extensible RNA-based gene-regulatory platform for engineering cellular function” by Maung Nyan Win and Christina D. Smolke (see pages 14283–14288)
ECOLOGY
A royal beckoning
The male honey bee's sole purpose is to mate with the queen honey bee, once, after which he dies. Even over long distances, the drone can sense the pheromone 9-oxo-2-decenoic acid (9-ODA), one of several substances the queen emits that control the colony's hierarchy, including female worker attentiveness and infertility. Using a functional genomics approach, Kevin Wanner et al. attempted to decipher whether 9-ODA is a purely sexual signal or also plays a role in social signaling, by searching for its receptor. The intricate nature of honey bee social behavior is controlled by pheromones released by the queen, but teasing out specific effects of each pheromone has been difficult. Functional genomics takes advantage of genome sequence data to identify molecular interactions. Wanner et al. found candidate pheromone receptors by looking for genes more highly expressed in drone antennae. The authors found that AmOr11 responds specifically to 9-ODA, showing that it is the likely receptor. The high degree of specificity suggests that AmOr11 is a pheromone receptor that mediates more than one behavioral effect, including influencing sexual and social behaviors. — T.H.D.
“A honey bee odorant receptor for the queen substance 9-oxo-2-decenoic acid” by Kevin W. Wanner, Andrew S. Nichols, Kimberly K. O. Walden, Axel Brockmann, Charles W. Luetje, and Hugh M. Robertson (see pages 14383–14388)
MEDICAL SCIENCES
Biomarker identified for Huntington's disease
Huntington's disease (HD), a hereditary neurodegenerative disorder, causes a progressive decline in mental and motor abilities, leading to abnormal involuntary movements, cognitive difficulties, and eventually death. Although it was one of the first inherited disorders to have an accurate genetic test, there are few reliable biomarkers for HD, which makes it difficult to predict disease onset or accurately measure progression. Current therapies for HD have been ineffective, and although many candidate treatments are in development, clinical trials of these agents require validated biomarkers. Toward this goal, Heike Runne et al. analyzed the up-regulation of neuroinflammatory genes in the blood of Huntington's patients. Neuroinflammation has been shown to be integral to the pathogenic process in the brain, and the tested genes included those involved in immune response and cell cycle and cell death pathways. One gene, immediate early response 3 (IER3), showed a significant increase in expression in patients' peripheral blood cells. The authors suggest that longitudinal studies may aid in the detection of additional HD biomarkers from readily available patient tissues and fluids, such as blood. — F.A.
“Analysis of potential transcriptomic biomarkers for Huntington's disease in peripheral blood” by Heike Runne, Alexandre Kuhn, Edward J. Wild, Wirahpati Pratyaksha, Mark Kristiansen, Jeremy D. Isaacs, Etienne Régulier, Mauro Delorenzi, Sarah J. Tabrizi, and Ruth Luthi-Carter (see pages 14424–14429)
NEUROSCIENCE
Mutant mouse models schizophrenia
Mice may be suitable model organisms for the study of physical disorders such as cardiovascular disease, but modeling of psychiatric diseases in rodents has proven much more difficult. Advances in the genetics of diseases such as schizophrenia have provided some promising candidate genes for such disorders, for example, the Disrupted-In-Schizophrenia gene DISC1. Takatoshi Hikida et al. describe their development and characterization of mice having a deficient version of this gene. DISC1 mutant mice had enlarged lateral ventricles, a feature frequently seen in patients with schizophrenia. The mice also displayed several behavioral abnormalities, including hyperactivity, disturbance in information processing, and depression-like symptoms, as well as a decrease in the protein marker associated with the abnormal electrical patterns observed in schizophrenia patients. Given the phenotypes of the DISC1 mutant mice and the converging genetic evidence linking DISC1 to a variety of psychiatric disorders, Hikida et al. suggest that these mice provide an important tool for further study of the combinations of factors that underlie major mental illnesses such as schizophrenia and mood disorders. — M.M.
“Dominant-negative DISC1 transgenic mice display schizophrenia-associated phenotypes detected by measures translatable to humans” by Takatoshi Hikida, Hanna Jaaro-Peled, Saurav Seshadri, Kenichi Oishi, Caroline Hookway, Stephanie Kong, Di Wu, Rong Xue, Manuella Andradé, Stephanie Tankou, Susumu Mori, Michela Gallagher, Koko Ishizuka, Mikhail Pletnikov, Satoshi Kida, and Akira Sawa (see pages 14501–14506)









