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<jats:p> Spatial models in ecology predict that populations may form patchy distributions within continuous habitats, through strong predator-prey or host-parasitoid interactions combined with limited dispersal. Empirical support of these models is provided. Parasitoids emanating from a population outbreak of tussock moths ( <jats:italic>Orgyia vetusta</jats:italic> ) suppressed the growth of nearby experimental populations of the moth, while experimental populations farther away were able to grow. This result explains the observed localized nature of tussock moth outbreaks and illustrates how population distributions can be regulated by dynamic spatial processes. </jats:p>

<jats:p>Theoretical research into the dynamics of coupled populations has suggested a rich ensemble of spatial structures that are created and maintained either by external disturbances or self-reinforcing interactions among the populations. Long-term data of the Canadian lynx from eight Canadian provinces display large-scale spatial synchrony in population fluctuations. The synchronous dynamics are not time-invariant, however, as pairs of populations that are initially in step may drift out of phase and back into phase. These observations are in agreement with predictions of a spatially-linked population model and support contemporary population ecology theory.</jats:p>

<jats:p> A lymphocyte subpopulation, the V <jats:sub>α</jats:sub> 14 natural killer T (NKT) cells, expresses both NK1.1 and a single invariant T cell receptor encoded by the V <jats:sub>α</jats:sub> 14 and J <jats:sub>α</jats:sub> 281 gene segments. Mice with a deletion of the J <jats:sub>α</jats:sub> 281 gene segment were found to exclusively lack this subpopulation. The V <jats:sub>α</jats:sub> 14 NKT cell–deficient mice could no longer mediate the interleukin-12 (IL-12)–induced rejection of tumors. Although the antitumor effect of IL-12 was thought to be mediated through natural killer cells and T cells, V <jats:sub>α</jats:sub> 14 NKT cells were found to be an essential target of IL-12, and they mediated their cytotoxicity by an NK-like effector mechanism after activation with IL-12. </jats:p>

<jats:p> Natural killer T (NKT) lymphocytes express an invariant T cell antigen receptor (TCR) encoded by the V <jats:sub>α</jats:sub> 14 and J <jats:sub>α</jats:sub> 281 gene segments. A glycosylceramide-containing α-anomeric sugar with a longer fatty acyl chain (C <jats:sub>26</jats:sub> ) and sphingosine base (C <jats:sub>18</jats:sub> ) was identified as a ligand for this TCR. Glycosylceramide-mediated proliferative responses of V <jats:sub>α</jats:sub> 14 NKT cells were abrogated by treatment with chloroquine–concanamycin A or by monoclonal antibodies against CD1d/V <jats:sub>β</jats:sub> 8, CD40/CD40L, or B7/CTLA-4/CD28, but not by interference with the function of a transporter-associated protein. Thus, this lymphocyte shares distinct recognition systems with either T or NK cells. </jats:p>

<jats:p>Signal transducers and activators of transcription (STATs) enhance transcription of specific genes in response to cytokines and growth factors. STAT1 is also required for efficient constitutive expression of the caspases Ice, Cpp32, and Ich-1 in human fibroblasts. As a consequence, STAT1-null cells are resistant to apoptosis by tumor necrosis factor α (TNF-α). Reintroduction of STAT1α restored both TNF-α–induced apoptosis and the expression of Ice, Cpp32, and Ich-1. Variant STAT1 proteins carrying point mutations that inactivate domains required for STAT dimer formation nevertheless restored protease expression and sensitivity to apoptosis, indicating that the functions of STAT1 required for these activities are different from those that mediate induced gene expression.</jats:p>

<jats:p> Transgenic <jats:italic>Drosophila</jats:italic> that expressed either luciferase or green fluorescent protein driven from the promoter of the clock gene <jats:italic>period</jats:italic> were used to monitor the circadian clock in explanted head, thorax, and abdominal tissues. The tissues (including sensory bristles in the leg and wing) showed rhythmic bioluminescence, and the rhythms could be reset by light. The photoreceptive properties of the explanted tissues indicate that unidentified photoreceptors are likely to contribute to photic signal transduction to the clock. These results show that autonomous circadian oscillators are present throughout the body, and they suggest that individual cells in <jats:italic>Drosophila</jats:italic> are capable of supporting their own independent clocks. </jats:p>

<jats:p>A family of homomultimeric outer-membrane proteins termed secretins mediates the secretion of large macromolecules such as enzymes and filamentous bacteriophages across bacterial outer membranes to the extracellular milieu. The secretin encoded by filamentous phage f1 was purified. Mass determination of individual molecules by scanning transmission electron microscopy revealed two forms, a unit multimer composed of about 14 subunits and a multimer dimer. The secretin is roughly cylindrical and has an internal diameter of about 80 angstroms, which is large enough to accommodate filamentous phage (diameter of 65 angstroms).</jats:p>

<jats:p>The nuclear factor of activated T cells (NFAT) group of transcription factors is retained in the cytoplasm of quiescent cells. NFAT activation is mediated in part by induced nuclear import. This process requires calcium-dependent dephosphorylation of NFAT caused by the phosphatase calcineurin. The c-Jun amino-terminal kinase (JNK) phosphorylates NFAT4 on two sites. Mutational removal of the JNK phosphorylation sites caused constitutive nuclear localization of NFAT4. In contrast, JNK activation in calcineurin-stimulated cells caused nuclear exclusion of NFAT4. These findings show that the nuclear accumulation of NFAT4 promoted by calcineurin is opposed by the JNK signal transduction pathway.</jats:p>

<jats:p> The <jats:italic>lethal yellow</jats:italic> ( <jats:italic> A <jats:sup>Y</jats:sup> /a </jats:italic> ) mouse has a defect in proopiomelanocortin (POMC) signaling in the brain that leads to obesity, and is resistant to the anorexigenic effects of the hormone leptin. It has been proposed that the weight-reducing effects of leptin are thus transmitted primarily by way of POMC neurons. However, the central effects of defective POMC signaling, and the absence of leptin, on weight gain in double-mutant <jats:italic>lethal yellow</jats:italic> ( <jats:italic> A <jats:sup>Y</jats:sup> /a </jats:italic> ) leptin-deficient ( <jats:italic> lep <jats:sup>ob</jats:sup> /lep </jats:italic> <jats:sup> <jats:italic>ob</jats:italic> </jats:sup> ) mice were shown to be independent and additive. Furthermore, deletion of the leptin gene restored leptin sensitivity to <jats:italic> A <jats:sup>Y</jats:sup> /a </jats:italic> mice. This result implies that in the <jats:italic> A <jats:sup>Y</jats:sup> /a </jats:italic> mouse, obesity is independent of leptin action, and resistance to leptin results from desensitization of leptin signaling. </jats:p>