Animals modify behavioral outputs in response to environmental changes. C. elegans exhibits thermotaxis, where well-fed animals show attraction to their cultivation temperature on a thermal gradient without food. We show here that feeding-state-dependent modulation of thermotaxis is a powerful behavioral paradigm for elucidating the mechanism underlying neural plasticity, learning, and memory in higher animals. Starved experience alone could induce aversive response to cultivation temperature. Changing both cultivation temperature and feeding state simultaneously evoked transient attraction to or aversion to the previous cultivation temperature: recultivation of starved animals with food immediately induced attraction to the temperature associated with starvation, although the animals eventually exhibited thermotaxis to the new temperature associated with food. These results suggest that the change in feeding state quickly stimulates the switch between attraction and aversion for the temperature in memory and that the acquisition of new temperature memory establishes more slowly. We isolated aho (a bnormal h unger o rientation) mutants that are defective in starvation-induced cultivation-temperature avoidance. Some aho mutants responded normally to changes in feeding state with respect to locomotory activity, implying that the primary thermosensation followed by temperature memory formation remains normal and the modulatory aspect of thermotaxis is specifically impaired in these mutants.A NIMALS can modulate behavioral responses by susbehavioral genetic approach to dissecting the molecular tained training and retain memory for a certain mechanism of learning and memory because of its accestime. Learning and memory have been successfully insible genetics (Brenner 1974), its stereotyped behavvestigated using model organisms such as Aplysia, Droioral responses, and the ease of controlling experimensophila, and mice. Various learning paradigms have tal conditions in the laboratory. C. elegans is also ideal for been developed in each model and analyzed behavior-

Aptamers selected against various kinds of targets have shown remarkable specificity and affinity, similar to those displayed by antibodies to their antigens. To employ aptamers as genotyping reagents for the identification of pathogens and their strains, in vitro selections were carried out to find aptamers that specifically bind and distinguish the closely related human influenza A virus subtype H3N2. The selected aptamer, P30-10-16, binds specifically to the haemagglutinin (HA) region of the target strain A/Panama/2007/1999(H3N2) and failed to recognize other human influenza viruses, including another strain with the same subtype, H3N2. The aptamer displayed over 15-fold-higher affinity to the HA compared with the monoclonal antibody, and efficiently inhibited HA-mediated membrane fusion. These studies delineate the application of aptamers in the genotyping of viruses.

Nickel (Ni) is an essential nutrient for plants, but excessive amounts can be toxic. Ni competes with iron (Fe) in vivo, raising the possibility that Ni is competitively taken up via the Fe uptake system in plants. Here, we show evidence that AtIRT1, the primary Fe(2+) uptake transporter in the root, mediates Ni accumulation in Arabidopsis thaliana. In hydroponic cultures, excess Ni exposure increased Fe accumulation and the relative transcription level of AtIRT1 in roots, indicating that excess Ni induces AtIRT1 expression in roots. An Fe-deficient treatment increased Ni accumulation in plants, suggesting that excess Ni was absorbed via the Fe uptake system, which was induced by Fe starvation. Moreover, Ni accumulation under Fe-deficient conditions was markedly lower in AtIRT1-defective mutants than in the wild-type, Col-0. Furthermore, AtIRT1 showed Ni(2+) uptake activity in a yeast expression system. These data demonstrate that AtIRT1 transports Ni(2+) in roots, and strongly suggest that Ni accumulation is further accelerated by AtIRT1 that is expressed in response to excess Ni.

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Although recent studies have provided significant molecular insights into the establishment of neuronal polarity in vitro, evidence is lacking on the corresponding phenomena in vivo, including correct localization of synaptic components and the importance of this process for function of the nervous system as a whole. RIA interneurons act as a pivotal component of the neural circuit for thermotaxis behavior in the nematode Caenorhabditis elegans and provide a suitable model to investigate these issues, having a neurite clearly divided into pre-and post-synaptic regions. In a screen for thermotaxis mutants, we identified the gene ttx-7, which encodes myo-inositol monophosphatase (IMPase), an inositol-producing enzyme regarded as a bipolar disorder-relevant molecule for its lithium sensitivity. Here we show that mutations in ttx-7 cause defects in thermotaxis behavior and localization of synaptic proteins in RIA neurons in vivo. Both behavioral and localization defects in ttx-7 mutants were rescued by expression of IMPase in adults and by inositol application, and the same defects were mimicked by lithium treatment in wild-type animals. These results suggest that IMPase is required in central interneurons of the mature nervous system for correct localization of synaptic components and thus for normal behavior.[Keywords: C. elegans; thermotaxis behavior; protein localization; synapse; myo-inositol monophosphatase; lithium] Supplemental material is available at http://www.genesdev.org. Received April 19, 2006; revised version accepted October 23, 2006. Neurons are the most highly polarized animal cell type and are composed of several subcellular compartments, including axons, dendrites, and cell bodies, each of which has its own molecular and physiological characteristics. How these polarized compartments are established has been extensively investigated using cultured hippocampal neurons as a model system (Dotti and Banker 1987;Dotti et al. 1988). Recent studies have demonstrated that GSK-3␤ and small GTPase-mediated signaling pathways are critical in assigning axonal fate to the immature neurite in hippocampal neurons (Arimura and Kaibuchi 2005;Jiang et al. 2005). The established axonal compartment is physically separated from the cell body by a molecular diffusional barrier, which is at least partly responsible for maintaining the distinct character of these two compartments (Nakada et al. 2003). However, it remains to be determined whether these mechanisms are common to all neuronal types or other mechanisms exist as well. Furthermore, to understand the physiological importance of polarization and consequent subcellular heterogeneity such as localization of synaptic proteins, it is essential to evaluate how these subcellular phenomena in vivo correlate with the function of neurons and the nervous system as a whole.The nematode Caenorhabditis elegans has a simple nervous system that consists of 302 neurons, the synaptic connectivity of which has been described in its entirety by electron microscopy (White et al...