Editors' Choice

Science  04 Feb 2005:
Vol. 307, Issue 5710, pp. 646

    Don't Keep Hedgehogs

    1. Caroline Ash

    Rescuing a hedgehog victim of a road accident and nurturing it back to health can be deeply satisfying. But Riley and Chomel show that the payback from such an exotic pet may not be entirely benign. Hedgehogs harbor a variety of pathogens that are potentially transferable to humans and our livestock. Several species of hedgehogs have been widely introduced into the United States and are kept illegally in some states, in the extraordinary number of 40,000 households. A recent survey shows that they can carry foot-and-mouth disease virus, Salmonella, and Mycobacteria, as well as dermal fungal infections. Thousands of years ago, domestication brought humans into contact with a range of new pathogens; the current vogue for exotic pets and food animals will do likewise, namely, monkeypox and plague in prairie dogs and SARS in civets.—CA

    Emerg. Infect. Dis. 11, 1 (2005).


    Popeye's Ribosomes

    1. Stella M. Hurtley

    Ribosomes are the central component of the protein synthesis machinery, and the efficient manufacture of ribosomes is crucial. These machines contain roughly 60 protein and RNA parts. The assembly of these parts occurs in the nucleus and involves importing proteins from the cytosol and placing them onto ribosomal RNA (rRNA); subsequently, the assembled small and large ribosomal subunits are exported to the cytosol.

    Two groups describe an unanticipated link in this chain of events—iron-sulfur (Fe-S) cluster biosynthesis. In a screen for ribosomal export mutants, Yarunin et al. found that genes implicated in Fe-S cluster biosynthesis in the cytosol are needed for ribosomal export. In particular, the protein Rli1 requires a Fe-S cluster to promote rRNA processing and small ribosomal subunit export. Kispal et al. also implicate Rli1 in the export of ribosomal subunits from the nucleus. In addition, they present evidence that this explains why Fe-S cluster biogenesis is an essential function and thus why mitochondria (where Fe-S cluster biogenesis originates) are essential. — SMH

    EMBO J. 10.1038/sj.emboj.7600540; 10.1038/sj.emboj.7600541 (2005).


    Unlocking Fluorescence

    1. Phillip D. Szuromi

    The power of fluorescent probes can be enhanced by controlling how and when the probe becomes excitable. Chandran et al. describe an approach for masking fluorescence from a xanthene fluorophore until it is cleaved by esterases within a cell. They coupled rhodamine 110 to two o-hydroxycinnamic acid derivatives via amide linkages. In their acetylated form, these side chains force the rhodamine core to adopt a nonfluorescing lactonized configuration. Ester cleavage causes the side chains to form a hydrocoumarin, which is favored by steric interaction of the methyl groups, and liberates the fluorescent acid form of rhodamine 110. The authors followed the uptake of the latent fluorophore into HeLa cells, where they observed strong fluorescence from the cytosol and lysosomes but not from the nucleus. — PDS

    J. Am. Chem. Soc. 10.1021/ja043736v (2005).


    Protection Against Erosion

    1. Brooks Hanson

    River and stream erosion rates and the resulting river profiles are becoming more widely recognized as depending on a complicated and incompletely documented suite of factors. For instance, some streams and rivers appear to be eroding their bedrock at the geologically extreme and unsustainable rates of several centimeters per year; hence, other processes must be contributing to bedrock dynamics. Over a 7-year period, Stock et al. monitored several rivers in Taiwan and in the Pacific Northwest of the United States. These rapidly eroding rivers had all been historically scoured of sediment. This history and the authors' measurements imply that long-term stream erosion, at least in areas with weak bedrock, is influenced more by the ability of rivers to entrain a thin covering of sediment, which reduces wear, than specific bedrock properties. In areas of high slope, debris flows, which periodically scour streams and rivers and thus allow rapid downcutting, may be the most critical factor. — BH

    Geol. Soc. Am. Bull. 117, 174 (2005).


    Less Editing, Less Depression

    1. Gilbert J. Chin

    A number of recent studies have fueled a sense of optimism that the fuzzy link between genes and behavior might be firmed up and made explicit, an especially challenging task given the likelihood that the contributions of individual genes (and distinct mutations) to behavior might be only a few percent of the total mix of predisposition, motivation, and environment. Biogenic amines are, of course, front and center in any consideration of mood and affect, and genes encoding various aspects of serotonin function in neurons (synthesis, transport, and receptors) have already been targeted as prime candidates for dysfunction in depression.

    Englander et al. have used a pair of mice strains to examine the interaction of serotonin receptors, stressful situations, and a selective serotonin reuptake inhibitor (SSRI). They report that, in comparison to C57BL/6 mice, BALB/c animals have lower serotonin levels (due to a polymorphism in tryptophan hydroxylase-2) and are generally easier to stress (via a behavioral despair task). Furthermore, the type 2C serotonin receptor in BALB/c mice undergoes less editing of its pre-messenger RNA, and this yields, in compensatory fashion, receptors that are more sensitive to serotonin. Administering the despair task or the SSRI (the antidepressant fluoxetine) bumps up the extent of RNA editing and presumably titrates downward the responsiveness of postsynaptic neurons to released serotonin. The unexpected finding is that this change in editing due to drug or stress is not seen if both are given together, suggesting that the molecular response may be influenced by the state of the subject and blocked by antidepressants. — GJC

    J. Neurosci. 25, 648 (2005).


    Getting a Fix on Fixation

    1. H. Jesse Smith

    Marine net primary production (NPP) is a measure of how much atmospheric carbon is fixed via photosynthesis by organisms in the ocean. Until now, only direct field sampling has yielded accurate estimates of NPP, which has severely limited attempts to obtain detailed global estimates of its distribution and magnitude. Measuring NPP from space has failed to provide convincing values, because two essential parameters, phytoplankton carbon biomass and a term related to the physiological status of the organisms, are not directly quantifiable remotely.

    Behrenfeld et al. start with satellite measurements of the chlorophyll content of upper ocean waters and the backscattering of certain wavelengths of light (which they use to estimate phytoplankton carbon biomass) and then estimate phytoplankton growth rates and calculate NPP. They can do this by taking advantage of laboratory studies that have shown that the ratio of chlorophyll to carbon biomass is a calculable function of changes in light, nutrients, and temperature. This work brings nearer the prospect of producing a more accurate picture of global marine NPP over space and time. — HJS

    Global Biogeochem. Cycles 19,

  7. STKE

    Balancing Axons and Dendrites

    1. Nancy Gough

    Neurons are polarized cells with axons (signal output) and dendrites (signal input). Not only are these functionally distinct parts of the cell, but they differ in morphology too. Jiang et al. report that when glycogen synthase kinase 3β (GSK-3β) activity was increased by transfection of isolated embryonic hippocampal neurons with a constitutively active mutant, the number of cells that formed an axon decreased, and when GSK-3β activity was inhibited, the number of cells producing multiple axons increased even though the overall number of neurites did not change. They identified the phosphatidylinositol 3-kinase (PI3K) pathway as a stimulator of GSK-3β phosphorylation, which results in an inhibition of GSK-3β. Activation of the PI3K pathway by expression of the kinase Akt or inactivation of the phosphatase PTEN produced multiaxon neurons. Yoshimura et al. show that GSK-3β phosphorylates collapsin response mediator protein 2 (CRMP-2), which is known to contribute to axon formation. Treatment of neurons with neurotrophin 3 (NT-3) or brain-derived neurotrophic factor (BDNF) stimulated axon growth and decreased CRMP-2 phosphorylation. Furthermore, the stimulation in axon length was blocked if CRMP-2 abundance was decreased. Thus, a pathway involving PI3K regulates the activity of GSK-3β and the phosphorylation of the microtubule assembly regulatory protein CRMP-2 and hence controls axon formation and growth in neurons.—NG

    Cell 120, 123; 137 (2005).

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