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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2010.10.003 Byline: Manojkumar A. Puthenveedu (1), Benjamin Lauffer (2), Paul Temkin (2), Rachel Vistein (1), Peter Carlton (3), Kurt Thorn (4), Jack Taunton (5), Orion D. Weiner (4), Robert G. Parton (6), Mark von Zastrow (2)(5) Keywords: CELLBIO; SIGNALING Abstract: The functional consequences of signaling receptor endocytosis are determined by the endosomal sorting of receptors between degradation and recycling pathways. How receptors recycle efficiently, in a sequence-dependent manner that is distinct from bulk membrane recycling, is not known. Here, in live cells, we visualize the sorting of a prototypical sequence-dependent recycling receptor, the beta-2 adrenergic receptor, from bulk recycling proteins and the degrading delta-opioid receptor. Our results reveal a remarkable diversity in recycling routes at the level of individual endosomes, and indicate that sequence-dependent recycling is an active process mediated by distinct endosomal subdomains distinct from those mediating bulk recycling. We identify a specialized subset of tubular microdomains on endosomes, stabilized by a highly localized but dynamic actin machinery, that mediate this sorting, and provide evidence that these actin-stabilized domains provide the physical basis for a two-step kinetic and affinity-based model for protein sorting into the sequence-dependent recycling pathway. Author Affiliation: (1) Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA, USA (2) Department of Psychiatry, University of California at San Francisco, San Francisco, CA 94158, USA (3) Department of Physiology, University of California at San Francisco, San Francisco, CA 94158, USA (4) Department of Biochemistry and Biophysics, University of California at San Francisco, San Francisco, CA 94158, USA (5) Department of Cellular and Molecular Pharmacology, University of California at San Francisco, San Francisco, CA 94158, USA (6) The University of Queensland, Institute for Molecular Bioscience and Centre for Microscopy and Microanalysis, St. Lucia, Queensland 4072, Australia 8 Article History: Received 31 October 2009; Revised 7 April 2010; Accepted 27 September 2010 Article Note: (miscellaneous) Published: November 24, 2010

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2010.09.011 Byline: Anke Bill (1), Anton Schmitz (1), Barbara Albertoni (1), Jin-Na Song (1), Lukas C. Heukamp (2), David Walrafen (3), Franziska Thorwirth (4), Peter J. Verveer (4), Sebastian Zimmer (2), Lisa Meffert (2), Arne Schreiber (3), Sampurna Chatterjee (5), Roman K. Thomas (5)(6)(7), Roland T. Ullrich (5), Thorsten Lang (3), Michael Famulok (1) Keywords: SIGNALING; HUMDISEASE Abstract: Signaling by ErbB receptors requires the activation of their cytoplasmic kinase domains, which is initiated by ligand binding to the receptor ectodomains. Cytoplasmic factors contributing to the activation are unknown. Here we identify members of the cytohesin protein family as such factors. Cytohesin inhibition decreased ErbB receptor autophosphorylation and signaling, whereas cytohesin overexpression stimulated receptor activation. Monitoring epidermal growth factor receptor (EGFR) conformation by anisotropy microscopy together with cell-free reconstitution of cytohesin-dependent receptor autophosphorylation indicate that cytohesins facilitate conformational rearrangements in the intracellular domains of dimerized receptors. Consistent with cytohesins playing a prominent role in ErbB receptor signaling, we found that cytohesin overexpression correlated with EGF signaling pathway activation in human lung adenocarcinomas. Chemical inhibition of cytohesins resulted in reduced proliferation of EGFR-dependent lung cancer cells in vitro and in vivo. Our results establish cytohesins as cytoplasmic conformational activators of ErbB receptors that are of pathophysiological relevance. Author Affiliation: (1) LIMES Institute, Program Unit Chemical Biology & Medicinal Chemistry, Laboratory of Chemical Biology, Rheinische Friedrich-Wilhelms-Universitat Bonn, Gerhard-Domagk-Str. 1, 53121 Bonn, Germany (2) Institute of Pathology, Universitatsklinikum, Rheinische Friedrich-Wilhelms-Universitat Bonn, Sigmund-Freud Strasse 25, 53123 Bonn, Germany (3) LIMES Institute, Program Unit Membrane Biology & Lipid Biochemistry, Laboratory of Membrane Biochemistry, Rheinische Friedrich-Wilhelms-Universitat Bonn, Carl-Troll-StraAe 31, 53115 Bonn, Germany (4) Department of Systemic Cell Biology, Max-Planck Institute of Molecular Physiology, Otto-Hahn-Str. 11, 44227 Dortmund, Germany (5) Max Planck Institute for Neurological Research with Klaus-Joachim-Zulch Laboratories of the Max Planck Society and the Medical Faculty of the University of Koln, Gleueler Str. 50, 50931 Koln, Germany (6) Chemical Genomics Centre of the Max Planck Society, Otto-Hahn Str. 15, 44227 Dortmund, Germany (7) Center of Integrated Oncology and Department I of Internal Medicine, University of Koln, Kerpener StraAe 62, 50937 Koln, Germany Article History: Received 20 April 2010; Revised 13 July 2010; Accepted 10 August 2010 Article Note: (miscellaneous) Published: October 14, 2010

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.tibs.2010.04.006 Byline: Lage Cerenius (1), Shun-ichiro Kawabata (2), Bok Luel Lee (3), Masaru Nonaka (4), Kenneth Soderhall (1) Abstract: Bacteria and other potential pathogens are cleared rapidly from the body fluids of invertebrates by the immediate response of the innate immune system. Proteolytic cascades, following their initiation by pattern recognition proteins, control several such reactions, notably coagulation, melanisation, activation of the Toll receptor and complement-like reactions. However, there is considerable variation among invertebrates and these cascades, although widespread, are not present in all phyla. In recent years, significant progress has been made in identifying and characterizing these cascades in insects. Notably, recent work has identified several connections and shared principles among the different pathways, suggesting that cross-talk between them may be common. Author Affiliation: (1) Department of Comparative Physiology, Uppsala University, Norbyvagen 18A, SE-752 36 Uppsala, Sweden (2) Department of Biology, Faculty of Sciences, Kyushu University, 6-10-1 Hakozaki, Higashi-Ku, Fukuoka 812-8581, Japan (3) National Research Laboratory of Defense Proteins, College of Pharmacy, Pusan National University, Jangjeon Dong, Gumjeong Gu, Busan 609-735, Korea (4) Department of Biological Sciences, Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2010.09.003 Byline: Tongda Xu (1), Mingzhang Wen (1), Shingo Nagawa (1), Ying Fu (1), Jin-Gui Chen (2), Ming-Jing Wu (2), Catherine Perrot-Rechenmann (3), JiAi Friml (4), Alan M. Jones (2)(5), Zhenbiao Yang (1) Keywords: SIGNALING; DEVBIO Abstract: Auxin is a multifunctional hormone essential for plant development and pattern formation. A nuclear auxin-signaling system controlling auxin-induced gene expression is well established, but cytoplasmic auxin signaling, as in its coordination of cell polarization, is unexplored. We found a cytoplasmic auxin-signaling mechanism that modulates the interdigitated growth of Arabidopsis leaf epidermal pavement cells (PCs), which develop interdigitated lobes and indentations to form a puzzle-piece shape in a two-dimensional plane. PC interdigitation is compromised in leaves deficient in either auxin biosynthesis or its export mediated by PINFORMED 1 localized at the lobe tip. Auxin coordinately activates two Rho GTPases, ROP2 and ROP6, which promote the formation of complementary lobes and indentations, respectively. Activation of these ROPs by auxin occurs within 30 s and depends on AUXIN-BINDING PROTEIN 1. These findings reveal Rho GTPase-based auxin-signaling mechanisms, which modulate the spatial coordination of cell expansion across a field of cells. Author Affiliation: (1) Center for Plant Cell Biology, Department of Botany and Plant Sciences, University of California, Riverside, CA 92521, USA (2) Department of Biology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA (3) Institut des Sciences du Vegetal, CNRS, UPR2355, 1 Avenue de la Terrasse, 91198 Gif sur Yvette Cedex, France (4) Department of Plant Systems Biology, VIB, and Department of Molecular Genetics, Ghent University, Technologiepark 927, 9052 Gent, Belgium (5) Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA Article History: Received 13 March 2010; Revised 2 June 2010; Accepted 30 July 2010 Article Note: (miscellaneous) Published: September 30, 2010

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2010.04.014 Byline: Anthony Otto (a), Raymond Macharia (b), Antonios Matsakas (a), Petr Valasek (a), Baljinder S. Mankoo (c), Ketan Patel (a) Keywords: Meox; Embryogenesis; Myogenesis; Skeletal; Muscle; Hypertrophy Abstract: The major component of skeletal muscle is the myofibre. Genetic intervention inducing over-enlargement of myofibres beyond a certain threshold through acellular growth causes a reduction in the specific tension generating capacity of the muscle. However the physiological parameters of a genetic model that harbours reduced skeletal muscle mass have yet to be analysed. Genetic deletion of Meox2 in mice leads to reduced limb muscle size and causes some patterning defects. The loss of Meox2 is not embryonically lethal and a small percentage of animals survive to adulthood making it an excellent model with which to investigate how skeletal muscle responds to reductions in mass. In this study we have performed a detailed analysis of both late foetal and adult muscle development in the absence of Meox2. In the adult, we show that the loss of Meox2 results in smaller limb muscles that harbour reduced numbers of myofibres. However, these fibres are enlarged. These myofibres display a molecular and metabolic fibre type switch towards a more oxidative phenotype that is induced through abnormalities in foetal fibre formation. In spite of these changes, the muscle from Meox2 mutant mice is able to generate increased levels of specific tension compared to that of the wild type. Author Affiliation: (a) School of Biological Sciences, Hopkins Building, University of Reading, Whiteknights Campus, Reading, Berkshire, RG6 6UB, UK (b) Royal Veterinary College, Royal College Street, NW1 0TU, London, UK (c) King's College London, Randall Division of Cell and Molecular Biophysics, New Hunt's House, Guy's Campus, London, SE1 1UL, UK Article History: Received 15 December 2009; Revised 24 March 2010; Accepted 12 April 2010

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.10.029 Byline: L. Feng (a)(b), R.E. Hernandez (a)(b)(c), J.S. Waxman (d), D. Yelon (d), C.B. Moens (a)(b) Keywords: Zebrafish; Retinoic acid; dhrs3; Retinoid metabolism; Negative feedback; Nervous system development; Hindbrain; rdh10 Abstract: Retinoic acid (RA) is an important developmental signaling molecule responsible for the patterning of multiple vertebrate tissues. RA is also a potent teratogen, causing multi-organ birth defects in humans. Endogenous RA levels must therefore be tightly controlled in the developing embryo. We used a microarray approach to identify genes that function as negative feedback regulators of retinoic acid signaling. We screened for genes expressed in early somite-stage embryos that respond oppositely to treatment with RA versus RA antagonists and validated them by RNA in situ hybridization. Focusing on genes known to be involved in RA metabolism, we determined that dhrs3a, which encodes a member of the short-chain dehydrogenase/reductase protein family, is both RA dependent and strongly RA inducible. Dhrs3a is known to catalyze the reduction of the RA precursor all-trans retinaldehyde to vitamin A; however, a developmental function has not been demonstrated. Using morpholino knockdown and mRNA over-expression, we demonstrate that Dhrs3a is required to limit RA levels in the embryo, primarily within the central nervous system. Dhrs3a is thus an RA-induced feedback inhibitor of RA biosynthesis. We conclude that retinaldehyde availability is an important level at which RA biosynthesis is regulated in vertebrate embryos. Author Affiliation: (a) Division of Basic Science and HHMI, Fred Hutchinson Cancer Research Center, B2-152, 1100 Fairview Ave. N, Seattle, WA 98109, USA (b) Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA, USA (c) Medical Scientist Training Program, University of Washington, Seattle, WA, USA (d) Developmental Genetics Program and Department of Cell Biology, Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016, USA Article History: Received 14 July 2009; Revised 13 October 2009; Accepted 21 October 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2009.10.012 Byline: Victor Serebruany (a), Ganesh Cherala (b), Craig Williams (b), Serge Surigin (a), Christopher Booze (a), Wiktor Kuliczkowski (c), Dan Atar (d) Abstract: Noncompliance is probably the major cause of clopidogrel 'resistance.' However, noncompliance is difficult to prove without confirming that the drug has been administered. Therefore, detection of plasma clopidogrel and/or metabolite(s) as the reliable objective method to confirm compliance is important. Author Affiliation: (a) HeartDrug Research Laboratories, Johns Hopkins University, Towson, MD (b) College of Pharmacy, Oregon State University/Oregon Health & Science University, Portland, OR (c) Silesian Center for Heart Diseases, Zabrze, Poland (d) Aker University Hospital, Div. of Cardiology, and Faculty of Medicine, Oslo, Norway Article History: Received 15 June 2009; Accepted 2 October 2009

To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1365-2745.2009.01568.x Byline: Duncan D. Cameron (1), Andy White (2), Janis Antonovics (1) Keywords: competition; diversity; food web; niche; nutrients; root hemi-parasite; species coexistence Abstract: Summary Parasitic plants affect the growth, reproduction and metabolism of their hosts and may also influence the outcome of competitive interactions between host species and, consequently, the structure of entire host communities. We investigate the effect of the root hemiparasitic plant Rhinanthus minor on plant community dynamics using a spatial theoretical model. The model is parameterized with data from pairwise interaction experiments under two nutrient levels between the hemiparasite and three grass species (Cynosurus cristatus, Festuca rubra and Phleum bertolonii) and three forb species (Leucanthemum vulgare, Plantago lanceolata and Ranunculus acris). Relative interaction coefficients were intransitive, with the dynamics of the system conforming to a rock-paper-scissors game. Stable deterministic dynamics emerge from parameters obtained under low-nutrient conditions. Under high-nutrient conditions, the dynamics are unstable, but are stabilized in spatially explicit models. The outcomes are sensitive to initial spatial pattern and frequency. Synthesis. This study supports the idea that hemiparasite populations may form 'shifting clouds' in natural populations and explains seemingly unpredictable shifts in host community structure following introduction of hemiparasites. Management of plant communities using hemiparasites needs to take these complex dynamics into account. Author Affiliation: (1)Department of Animal and Plant Sciences, University of Sheffield, Alfred Denny Building, Western Bank, Sheffield S10 2TN, UK (2)Department of Mathematics and Maxwell Institute for Mathematical Sciences, Heriot Watt University, Edinburgh EH14 4AS, UK Article History: Received 7 November 2008; accepted 7 August 2009 Handling Editor: Bryan Foster Article note: (*) Correspondence author. E-mail: d.cameron@shef.ac.uk

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.06.013 Byline: Xiaoyun Yang (a), Markus Weber (b), Nazanin ZarinKamar (a), Nico Posnien (c)(d), Frank Friedrich (e), Barbara Wigand (b), Rolf Beutel (e), Wim G.M. Damen (f), Gregor Bucher (c)(d), Martin Klingler (b), Markus Friedrich (a)(g) Keywords: Eyeless; Twin of eyeless; Dachshund; Tribolium; Evolution of development; Eye development; Redundancy; Retinal determination gene network; Drosophila Abstract: The Pax6 genes eyeless (ey) and twin of eyeless (toy) are upstream regulators in the retinal determination gene network (RDGN), which instructs the formation of the adult eye primordium in Drosophila. Most animals possess a singleton Pax6 ortholog, but the dependence of eye development on Pax6 is widely conserved. A rare exception is given by the larval eyes of Drosophila, which develop independently of ey and toy. To obtain insight into the origin of differential larval and adult eye regulation, we studied the function of toy and ey in the red flour beetle Tribolium castaneum. We find that single and combinatorial knockdown of toy and ey affect larval eye development strongly but adult eye development only mildly in this primitive hemimetabolous species. Compound eye-loss, however, was provoked when ey and toy were RNAi-silenced in combination with the early retinal gene dachshund (dac). We propose that these data reflect a role of Pax6 during regional specification in the developing head and that the subsequent maintenance and growth of the adult eye primordium is regulated partly by redundant and partly by specific functions of toy, ey and dac in Tribolium. The results from embryonic knockdown and comparative protein sequence analysis lead us further to conclude that Tribolium represents an ancestral state of redundant control by ey and toy. Author Affiliation: (a) Department of Biological Sciences, Wayne State University, 5047 Gullen Mall, Detroit, MI 48202, USA (b) Institut fur Zoologie, Friedrich-Alexander-Universitat Erlangen, Staudtstr. 5, 91058 Erlangen, Germany (c) Blumenbach Institut fur Zoologie und Anthropologie Georg-August-Universitat Gottingen, Justus-von-Liebig-Weg 11, 37077 Gottingen, Germany (d) DFG Research Center for the Molecular Physiology of the Brain (CMPB), Germany (e) Institut fur Spezielle Zoologie und Evolutionsbiologie, Friedrich Schiller Universitaet Jena, Erbertstrasse 1, 07743 Jena, Germany (f) Institut fur Genetik, Universitat zu Koln, Weyertal 121, D-50931 Koln, Germany (g) Department of Anatomy and Cell Biology, Wayne State University, School of Medicine, 540 East Canfield Avenue, Detroit, MI 48201, USA Article History: Received 26 February 2009; Revised 18 May 2009; Accepted 7 June 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.addbeh.2009.05.010 Byline: Jean-Francois Etter (a), Jean-Charles Hoda (b), Nader Perroud (c), Marcus MunafA[sup.2] (d), Catherine Buresi (c), Claudette Duret (b), Elisabeth Neidhart (b)(c), Alain Malafosse (c), Daniel Bertrand (b) Keywords: Genetics; Nicotine dependence; Nicotinic receptors; Cigarette smoking Abstract: We assessed whether smoking behavior was associated with nine polymorphisms in genes coding for the nicotinic receptor subunits [alpha]-4 (rs1044394, rs1044396, rs2236196 and rs2273504), [alpha]-5 (rs16969968), [beta]-2 (rs2072661 and rs4845378) and [beta]-3 (rs4953 and rs6474413). We conducted an Internet survey and collected saliva by mail for DNA and cotinine analyses, in Switzerland in 2003. We conducted DNA analyses for 277 participants and cotinine analyses for 141 current daily smokers. Cotinine levels were higher in carriers of the CC genotype of CHRNA4 rs1044396 (371 ng/ml) than in those with the CT or TT genotypes (275 ng/ml, p =0.049), a difference of 0.53 standard deviation units. However, this difference was not robust to correction for multiple testing using Bonferroni adjustment. These 9 polymorphisms were not otherwise associated with smoking behavior and nicotine dependence. There were possible associations between the temperament trait novelty seeking and CHRNA4 rs1044396, CHRNA5 rs16969968 and CHRNB2 rs4845378, but these associations were not robust to correction for multiple testing. We conclude that the analysis of polymorphisms in genes coding for four nicotinic acetylcholine receptor subunits (CHRNA4, CHRNA5, CHRNB2 and CHRNB3) and several smoking-related phenotypes revealed no statistically significant association. Author Affiliation: (a) Institute of Social and Preventive Medicine, Faculty of Medicine, University of Geneva, CMU, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland (b) Department of Physiology, Faculty of Medicine, University of Geneva, 1211 Geneva 4, Switzerland (c) Department of Genetic Medicine and Development, Geneva University Hospitals, 1211 Geneva 4, Switzerland (d) Department of Experimental Psychology, University of Bristol, Bristol, BS8 1TU, U.K.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.05.576 Byline: Enrico Moro (a), Lara Gnugge (b), Paola Braghetta (c), Marino Bortolussi (a), Francesco Argenton (a) Keywords: Zebrafish; Pancreas; Insulin; Beta cell; Self-replication; Conditional ablation; Time lapse confocal microscopy Abstract: Among the different mechanisms invoked to explain the beta cell mass expansion during postnatal stages and adulthood, self-replication is being considered the major cellular event occurring both under physiological conditions and in regenerating pancreas after partial pancreactomy. Neogenesis, i.e. differentiation from pancreatic progenitors, has been demonstrated to act concurrently with beta cell replication during pancreatic regeneration. Both phenomena have been largely elucidated in higher vertebrates (mouse, rat and guinea pig), but an extensive description of beta cell dynamics in other animal models is currently lacking. We, therefore, explored in zebrafish the cellular origins of new beta cells in both adult and larval stages. By integrating the results from in vivo time lapse analysis and immunostaining, we provide a detailed reconstruction of the major processes involved in fish beta cell genesis and maintenance. Moreover, by establishing the selective ablation of proliferating beta cells, through the ganciclovir-HSVTK system, we could show that in larval stages self-replication is the main mechanism of beta cells expansion. Since the same mechanism of proliferation has been observed to occur during early and late life stages, we suggest that zebrafish larvae can be used as an alternative tool for an in vivo exploration and screening of new potential mitogens specifically targeting beta cells. Author Affiliation: (a) Department of Biology, University of Padova, I-35121 Padova, Italy (b) Developmental Biology, Institute Biology 1, University of Freiburg, Hauptstrasse 1, D-79104 Freiburg, Germany (c) Department of Histology, Microbiology, and Medical Biotechnologies, I-35121 Padova, Italy Article History: Received 2 September 2008; Revised 28 May 2009; Accepted 29 May 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2009.05.036 Byline: Manu V. Chakravarthy (1), Irfan J. Lodhi (1), Li Yin (1), Raghu R.V. Malapaka (3), H. Eric Xu (3), John Turk (1), Clay F. Semenkovich (1)(2) Keywords: PROTEINS; SIGNALING; HUMDISEASE Abstract: The nuclear receptor PPAR[alpha] is activated by drugs to treat human disorders of lipid metabolism. Its endogenous ligand is unknown. PPAR[alpha]-dependent gene expression is impaired with inactivation of fatty acid synthase (FAS), suggesting that FAS is involved in generation of a PPAR[alpha] ligand. Here we demonstrate the FAS-dependent presence of a phospholipid bound to PPAR[alpha] isolated from mouse liver. Binding was increased under conditions that induce FAS activity and displaced by systemic injection of a PPAR[alpha] agonist. Mass spectrometry identified the species as 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine (16:0/18:1-GPC). Knockdown of Cept1, required for phosphatidylcholine synthesis, suppressed PPAR[alpha]-dependent gene expression. Interaction of 16:0/18:1-GPC with the PPAR[alpha] ligand-binding domain and coactivator peptide motifs was comparable to PPAR[alpha] agonists, but interactions with PPAR[delta] were weak and none were detected with PPAR[gamma]. Portal vein infusion of 16:0/18:1-GPC induced PPAR[alpha]-dependent gene expression and decreased hepatic steatosis. These data suggest that 16:0/18:1-GPC is a physiologically relevant endogenous PPAR[alpha] ligand. Author Affiliation: (1) Endocrinology, Metabolism, and Lipid Research, Department of Medicine, Washington University School of Medicine, Campus Box 8127, 660 South Euclid Avenue, St. Louis, MO 63110, USA (2) Department of Cell Biology and Physiology, Washington University School of Medicine, Campus Box 8127, 660 South Euclid Avenue, St. Louis, MO 63110, USA (3) Laboratory of Structural Sciences, Van Andel Research Institute, 333 Bostwick Avenue, Grand Rapids, MI 49503, USA Article History: Received 29 August 2008; Revised 10 March 2009; Accepted 7 May 2009 Article Note: (miscellaneous) Published online: July 30, 2009

Byline: Barbara KAapciAska (1), Ewa Sadowska-KrApa (1), SAawomir Jagsz (1), Andrzej Sobczak (2), MaAgorzata A>>endzian-Piotrowska (3), Jan Gorski (3), Jozef Langfort (1,4) Keywords: Left ventricular hypertrophy; Tachycardia; Rat Abstract: Increased oxidative stress resulting from enhanced production of reactive oxygen species and/or inadequate mechanisms of antioxidant defenses has been recognized as an important factor contributing to the initiation and progression of cardiac dysfunction under a wide variety of pathophysiological conditions. The main objective of this study was to examine the effect of electrically induced tachycardia on oxidative stress and the capacity of antioxidant defenses in the normal and hypertrophied left ventricle (LV) in the rat. Left ventricular hypertrophy (LVH) was produced by banding the descending abdominal aorta. The activities of antioxidant enzymes, concentrations of non-enzymatic antioxidants, and biomarkers of oxidative stress were measured in the LV of aortic-banded animals (LVH), untreated or banded rats subjected to short-term (45 min) atrial pacing [(CTR + S) and (LVH + S), respectively], and untreated (CTR) or sham-operated (SHAM) controls. The results indicate that the increase in heart rate in vivo as a result of atrial pacing to a maximum level, independent of sympathetic nerve activity, leads to a substantial increase in oxidative stress and a marked decline in the activities of antioxidant enzymes in both the normal and hypertrophied left ventricle of the rat. The accompanying increase in tissue content of [alpha]- and I3-tocopherols seem to contribute to attenuation of the oxidant stress-related loss of thiol stores in the LV. Stable left ventricular hypertrophy induced by aortic banding for six weeks has a minor impact on the capacity of the endogenous antioxidant defense system in the LV, but significantly and negatively affects the ability of the heart LV to tolerate the stress of tachycardia. Author Affiliation: (1) Department of Physiological and Medical Sciences, Academy of Physical Education, 72A MikoAowska Str, 40-065, Katowice, Poland (2) Department of General and Inorganic Chemistry, School of Pharmacy, The Medical University of Silesia, Sosnowiec, Poland (3) Department of Physiology, Medical University of Bialystok, 2c Mickiewicza Str., BiaAystok, Poland (4) Department of Experimental Pharmacology, Polish Academy of Sciences Medical Research Center, Warsaw, Poland Article History: Registration Date: 02/02/2009 Received Date: 25/11/2008 Accepted Date: 29/01/2009 Online Date: 26/02/2009 Article note: An erratum to this article can be found online at http://dx.doi.org/10.1007/s12576-012-0242-7.

To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1365-2745.2008.01477.x Byline: Suzanne B. Boyden (1,2), Peter B. Reich (1), Klaus J. Puettmann (1,3), Timothy R. Baker (1,4) Keywords: competition; density; ontogeny; over-yielding; rank reversals; sapling growth; shade-tolerance; succession Abstract: Summary Rank reversals in species performance are theoretically important for structuring communities, maintaining diversity and determining the course of forest succession. Species growth ranks can change with ontogeny or in different microenvironments, but interactions between ontogeny and the environment are not well-understood because of the lack of long-term forest competition studies. While early differences in growth among species may reflect intrinsic differences in shade-tolerance and physiology, ontogenetic trends in growth and variation in neighbourhood density and composition may change or even reverse early patterns of growth rankings. We experimentally studied spatial and temporal patterns of species interactions and growth for three northern tree species: Larix laricina, Picea mariana and Pinus strobus. We compared species size and growth rankings over an 11-year period, for different species mixtures planted at four density levels in north-eastern Minnesota, USA. The benefits of different growth strategies changed with ontogeny and density leading to reversals in the size rank of competing species over time and space. High-density stands promoted dominance and resource pre-emption by L. laricina, whereas lower-density stands favoured gradual accumulation of biomass and eventual dominance by P. strobus. In the absence of strong neighbour competition, ontogenetic trends in growth had greater influence on growth patterns. Species interactions affected the productivity of mixed stands vs. monocultures. Species generally grew more in monoculture than when planted with P. strobus at low density, or with L. laricina at high density. Only L. laricina and P. mariana showed potential for greater overall productivity, or over-yielding, when planted together than alone, probably because of improved resource uptake by the highly stratified canopy. Synthesis. Density predictably determined whether size-asymmetric growth or ontogenetic growth trends would drive early establishment and growth patterns. Variation in vertical and horizontal structure that results from early competitive dynamics can influence the successional trajectory or character of the mature forest. This study extends previous efforts to identify the causes of rank reversals in communities and understand the importance of temporal changes beyond the early years of seedling establishment. Author Affiliation: (1)Department of Forest Resources, University of Minnesota, St. Paul, MN 55108, USA; (2)Department of Biology, Clarion University, Clarion, PA 16214, USA; (3)Department of Forest Sciences, Oregon State University, Corvallis, OR 97331, USA; and (4)Forestry and Natural Resources, College of the Redwoods, Eureka, CA 95501, USA Article History: Received: 29 May 2008; accepted: 10 December 2008 Handling Editor: Susan Schwinning Article note: (*) Correspondence author. E-mail: sboyden@clarion.edu

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.anbehav.2008.10.028 Byline: Richard B. D'Eath (a), Bert J. Tolkamp (b), Ilias Kyriazakis (c), Alistair B. Lawrence (a) Abstract: In animals, including humans, free access to high-quality (generally energy-dense) food can result in obesity, leading to physiological and health problems. Consequently, various captive animals, including laboratory and companion animals and certain farm animals, are often kept on a restricted diet. Quantitative restriction of food is associated with signs of hunger such as increases in feeding motivation, activity and redirected oral behaviours which may develop into stereotypies. An alternative approach to energy intake restriction is to provide more food, but of a reduced quality. Such alternative diets are usually high in fibre and have lower energy density. The benefits of these alternative diets for animals are controversial: some authors argue that they result in more normal feeding behaviour, promote satiety and so improve animal welfare; others argue that 'metabolic hunger' remains no matter how the restriction of energy intake and weight gain is achieved. We discuss the different arguments behind this controversy, focusing on two well-researched cases of food-restricted farmed livestock: pregnant sows and broiler breeders. Disagreement between experts results from differences in assumptions about what determines and controls feeding behaviour and food intake, from the methodology of assessing animal hunger and from the weighting placed on 'naturalness' of behaviour as a determinant of welfare. Problems with commonly used behavioural and physiological measures of hunger are discussed. Future research into animal feeding preferences, in particular the relative weight placed on food quantity and quality, would be valuable, alongside more fundamental research into the changes in feeding physiology associated with alternative diets. Author Affiliation: (a) Animal Behaviour and Welfare Department, Scottish Agricultural College, Edinburgh, U.K. (b) Animal Nutrition and Health Department, Scottish Agricultural College, Edinburgh, U.K. (c) Veterinary Faculty, University of Thessaly, Greece Article History: Received 11 June 2007; Revised 1 September 2008; Accepted 20 October 2008 Article Note: (miscellaneous) MS. number: RV-74

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1523-1739.2008.01035.x Byline: K. S. GOBUSH (*[double dagger]), B. M. MUTAYOBA ([dagger]), S. K. WASSER (*) Keywords: gene-drop analysis; glucocorticoids; Loxodonta africana; microsatellite DNA; poaching; relatedness Abstract: Abstract: Widespread poaching prior to the 1989 ivory ban greatly altered the demographic structure of matrilineal African elephant (Loxodonta africana) family groups in many populations by decreasing the number of old, adult females. We assessed the long-term impacts of poaching by investigating genetic, physiological, and reproductive correlates of a disturbed social structure resulting from heavy poaching of an African elephant population in Mikumi National Park, Tanzania, prior to 1989. We examined fecal glucocorticoid levels and reproductive output among 218 adult female elephants from 109 groups differing in size, age structure, and average genetic relatedness over 25 months from 2003 to 2005. The distribution in group size has changed little since 1989, but the number of families with tusked old matriarchs has increased by 14.2%. Females from groups that lacked an old matriarch, first-order adult relatives, and strong social bonds had significantly higher fecal glucocorticoid values than those from groups with these features (all females R.sup.2= 0.31; females in multiadult groups R.sup.2= 0.46). Females that frequented isolated areas with historically high poaching risk had higher fecal glucocorticoid values than those in low poaching risk areas. Females with weak bonds and low group relatedness had significantly lower reproductive output (R.sup.2[U]=0.21). Females from disrupted groups, defined as having observed average group relatedness 1 SD below the expected mean for a simulated unpoached family, had significantly lower reproductive output than females from intact groups, despite many being in their reproductive prime. These results suggest that long-term negative impacts from poaching of old, related matriarchs have persisted among adult female elephants 1.5 decades after the 1989 ivory ban was implemented. Abstract (Spanish): Impactos a Largo Plazo de la Caceria Furtiva sobre el Grado de Relacion, la Fisiologia del Estres y la Productividad de Hembras Adultas de Elefantes Africanos Resumen: La caceria furtiva generalizada antes de la prohibicion del comercio de marfil en 1989 altero la estructura demografica de grupos familiares matrilineales de elefante africano (Loxodonta africana) en muchas poblaciones por la disminucion del numero de hembras adultas, viejas. Evaluamos los impactos a largo plazo de la caceria furtiva investigando correlaciones geneticas, fisiologicas y reproductivas de una estructura social perturbada resultante de la caceria furtiva intensiva de una poblacion de elefante africano en el Parque Nacional Mikumi, Tanzania, antes de 1989. Examinamos los niveles de glucocorticoides fecales y la productividad de 218 hembras adultas de 109 grupos de diferente tamano, estructura de edades y relacion genetica promedio durante 25 meses entre 2003 y 2005. La distribucion del tamano de los grupos ha cambiado poco desde 1989, pero el numero de familias con matriarcas viejas con colmillos ha incrementado en 14.2%. Las hembras de grupos que carecian de una matriarca vieja, parientes adultos de primer orden y lazos sociales estrechos tenian valores de glucocorticoides significativamente mayores que los grupos con esas caracteristicas (todas las hembras R.sup.2= 0.31; hembras en grupos multiadultos R.sup.2= 0.46). Las hembras que frecuentaban lugares aislados con riesgo historicamente alto de caza furtiva tuvieron niveles de glucocorticoides mas altos que en las areas con bajo riesgo de caza furtiva. Las hembras con relaciones debiles y un bajo grado de relacion entre grupos tuvieron una productividad significativamente menor (R.sup.2[U]=0.21). Las hembras de grupos desestabilizados, definidas con base en un grado observado de relacion entre grupos 1 DS debajo de la media esperada para una familia no cazada simulada, tuvieron una productividad significativamente menor que las hembras de grupos intactos, no obstante que muchas estaban en su mejor momento reproductivo. Estos resultados sugieren que los impactos negativos a largo plazo de la caceria de matriarcas viejas emparentadas han persistido entre las hembras adultas jovenes 1.5 decadas despues de la prohicion del comercio de marfil. Author Affiliation: (*)Department of Biology, University of Washington, Box 351800, Seattle, Washington 98195-1800, U.S.A. ([dagger])Faculty of Veterinary Medicine, Sokoine University of Agriculture, Box 3015 Chuo Kikuu, Morogoro, Tanzania Article History: Paper submitted October 23, 2007; revised manuscript accepted March 13, 2008. Article note: ([double dagger]) email gobush@u.washington.edu

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2006.10.032 Byline: Sang-Wook Kang (1), Neena S. Rane (1), Soo Jung Kim (2), Jennifer L. Garrison (3), Jack Taunton (3), Ramanujan S. Hegde (1) Abstract: Eukaryotic proteins entering the secretory pathway are translocated into the ER by signal sequences that vary widely in primary structure. We now provide a functional rationale for this long-observed sequence diversity by demonstrating that differences among signals facilitate substrate-selective modulation of protein translocation. We find that during acute ER stress, translocation of secretory and membrane proteins is rapidly and transiently attenuated in a signal sequence-selective manner. Their cotranslational rerouting to the cytosol for degradation reduces the burden of misfolded substrates entering the ER and represents a pathway for pre-emptive quality control (pQC). Bypassing the pQC pathway for the prion protein increases its rate of aggregation in the ER lumen during prolonged stress and renders cells less capable of viable recovery. Conversely, pharmacologically augmenting pQC during ER stress proved protective. Thus, protein translocation is a physiologically regulated process that is utilized for pQC as part of the ER stress response. Author Affiliation: (1) Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, 18 Library Drive, Building 18T, Room 101, Bethesda, MD, 20892, USA (2) Functional Genomic Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 305-333, Korea (3) Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA, 94107, USA Article History: Received 14 June 2006; Revised 30 August 2006; Accepted 4 October 2006 Article Note: (miscellaneous) Published: November 30, 2006

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2006.09.012 Byline: Antonio Fernandez-Guerra (a), Antoine Aze (a), Julia Morales (b), Odile Mulner-Lorillon (b), Bertrand Cosson (b), Patrick Cormier (b), Cynthia Bradham (c), Nikki Adams (d), Anthony J. Robertson (e), William F. Marzluff (f), James A. Coffman (e), Anne-Marie Geneviere (a) Keywords: Sea urchin; Cell cycle; Replication; Mitosis; Checkpoint; Kinases Abstract: A search of the Strongylocentrotus purpuratus genome for genes associated with cell cycle control and DNA metabolism shows that the known repertoire of these genes is conserved in the sea urchin, although with fewer family members represented than in vertebrates, and with some cases of echinoderm-specific gene diversifications. For example, while homologues of the known cyclins are mostly encoded by single genes in S. purpuratus (unlike vertebrates, which have multiple isoforms), there are additional genes encoding novel cyclins of the B and K/L types. Almost all known cyclin-dependent kinases (CDKs) or CDK-like proteins have an orthologue in S. purpuratus; CDK3 is one exception, whereas CDK4 and 6 are represented by a single homologue, referred to as CDK4. While the complexity of the two families of mitotic kinases, Polo and Aurora, is close to that found in the nematode, the diversity of the NIMA-related kinases (NEK proteins) approaches that of vertebrates. Among the nine NEK proteins found in S. purpuratus, eight could be assigned orthologues in vertebrates, whereas the ninth is unique to sea urchins. Most known DNA replication, DNA repair and mitotic checkpoint genes are also present, as are homologues of the pRB (two) and p53 (one) tumor suppressors. Interestingly, the p21/p27 family of CDK inhibitors is represented by one homologue, whereas the INK4 and ARF families of tumor suppressors appear to be absent, suggesting that these evolved only in vertebrates. Our results suggest that, while the cell cycle control mechanisms known from other animals are generally conserved in sea urchin, parts of the machinery have diversified within the echinoderm lineage. The set of genes uncovered in this analysis of the S. purpuratus genome should enhance future research on cell cycle control and developmental regulation in this model. Author Affiliation: (a) Observatoire Oceanologique de Banyuls-Laboratoire Arago, CNRS-UMR7628/UPMC, 66650 Banyuls-sur-Mer, France (b) Station Biologique de Roscoff, CNRS-UMR7150/UPMC, 29680 Roscoff, France (c) Developmental, Cellular, and Molecular Biology Group, Duke University, Durham, NC, USA (d) Department of Biological Sciences, California Polytechnic State University, San Luis Obispo, CA, USA (e) Mount Desert Island Biological Laboratory, Salisbury Cove, ME, USA (f) Program in Molecular Biology, University of North Carolina, Chapel Hill, NC, USA Article History: Received 30 May 2006; Revised 6 September 2006; Accepted 7 September 2006

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2006.08.046 Byline: Wendy S. Beane (a), Ekaterina Voronina (b), Gary M. Wessel (b), David R. McClay (a) Keywords: Ras GTPase; Rho; G protein; Galpha; Dynamin; SRP; Signal recognition particle receptor; Translation; Gene duplication; Phylogenomics; Echinoderm Abstract: In every organism, GTP-binding proteins control many aspects of cell signaling. Here, we examine in silico several GTPase families from the Strongylocentrotus purpuratus genome: the monomeric Ras superfamily, the heterotrimeric G proteins, the dynamin superfamily, the SRP/SR family, and the 'protein biosynthesis' translational GTPases. Identified were 174 GTPases, of which over 90% are expressed in the embryo as shown by tiling array and expressed sequence tag data. Phylogenomic comparisons restricted to Drosophila, Ciona, and humans (protostomes, urochordates, and vertebrates, respectively) revealed both common and unique elements in the expected composition of these families. G[alpha] and dynamin families contain vertebrate expansions, consistent with whole genome duplications, whereas SRP/SR and translational GTPases are highly conserved. Unexpectedly, Ras superfamily analyses revealed several large (5+) lineage-specific expansions in the sea urchin. For Rho, Rab, Arf, and Ras subfamilies, comparing total human gene numbers to the number of sea urchin genes with vertebrate orthologs suggests reduced genomic complexity in the sea urchin. However, gene duplications in the sea urchin increase overall numbers such that total sea urchin gene numbers approximate vertebrate gene numbers for each monomeric GTPase family. These findings suggest that lineage-specific expansions may be an important component of genomic evolution in signal transduction. Author Affiliation: (a) Department of Biology, Developmental, Cell and Molecular Group, Duke University, Box 91000, Durham, NC 27708, USA (b) Department of Molecular and Cell Biology and Biochemistry, Brown University, 69 Brown Street, Providence, RI 02912, USA Article History: Received 11 May 2006; Revised 18 August 2006; Accepted 19 August 2006

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.tips.2006.06.004 Byline: Anne E. King (1), Michael A. Ackley (2), Carol E. Cass (3)(4), James D. Young (5), Stephen A. Baldwin (1) Abstract: Hydrophilic purine and pyrimidine nucleosides rely on specialized carrier proteins for their membrane translocation. The recent identification of two gene families encoding equilibrative and concentrative nucleoside transporters in mammals and other organisms has provided the essential breakthrough to a more complete understanding of the biological significance of nucleoside transport. Although nucleoside salvage is a primary function of these proteins, recent data indicate functions beyond metabolic recycling. In brain and spinal cord, for example, nucleoside transporters have the potential to regulate synaptic levels of neuroactive purines such as adenosine and, thereby, indirectly modulate physiological processes through G-protein-coupled purine P1 receptors. As described in this review, recent research indicates novel putative functions for CNS nucleoside transporters in sleep, arousal, drug and alcohol addiction, nociception and analgesia. The therapeutic use of nucleoside analogue drugs and nucleoside transporter inhibitors in viral, neoplastic, cardiovascular and infectious disease is also described. Author Affiliation: (1) Institute of Membrane and Systems Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK (2) Pfizer Global R&D, Sandwich, Kent CT13 9NJ, UK (3) Membrane Protein Research Group, Department of Oncology, University of Alberta, Alberta T6G 2H7, Canada (4) Cross Cancer Institute, Edmonton, Alberta T6G 2H7, Canada (5) Membrane Protein Research Group, Department of Physiology, University of Alberta, Alberta T6G 2H7, Canada

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.dsr.2006.05.008 Byline: Rui Company (a), Angela Serafim (a), Richard Cosson (b), Aline Fiala-Medioni (c), David Dixon (d), Maria Joao Bebianno (a) Abstract: Hydrothermal vent mussels are exposed continually to toxic compounds, including high metal concentrations and other substances like dissolved sulphide, methane and natural radioactivity. Fluctuations in these parameters appear to be common because of the characteristic instability of the hydrothermal environment. Temporal variation in the antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), total glutathione peroxidases (Total GPx), selenium dependent glutathione peroxidases (Se-GPx)), metallothioneins and lipid peroxidation (LPO) in the gills and mantle of the mussel Bathymodiolus azoricus from Menez-Gwen hydrothermal vent site was evaluated and related to the accumulated metal concentrations (Ag, Cu, Cd, Fe, Mn and Zn) in the tissues. Maximum antioxidant enzyme activities in the gills were detected in the beginning of summer, followed by a gradual decrease throughout the following months. One year after, the levels of antioxidant enzyme activities were similar to those reported one year before. LPO in this tissue exhibited a similar temporal variation trend. A different pattern of temporal variation in antioxidant enzyme activities was observed in the mantle, with a gradual increase from summer to the end of autumn (November). LPO in the mantle exhibited an almost reverse trend of temporal variation to that of antioxidant enzyme activities in this tissue. Antioxidant defences in the gills of B. azoricus were significantly enhanced with increasing concentrations of Ag, Cu and Mn, while negative relationships between antioxidant enzymes and Cd, Cu, Mn and Zn concentrations in the mantle were observed, suggesting different pathways of reactive oxygen species (ROS) production and that these tissues responded differently to the metal accumulation. However, temporal variation in biomarkers of defence and damage were in general similar to coastal bivalve species and can be associated with temporal variations of the physiological status due to reproduction. These variations might also be linked to the highly unstable nature of the hydrothermal environment. Author Affiliation: (a) CIMA, Faculty of Marine and Environmental Sciences, University of Algarve, Campus de Gambelas, 8000 Faro, Portugal (b) ISOMer-UPRES-EA 2663, Laboratoire de Biologie Marine, Faculte des Sciences et Techniques, Universite de Nantes, BP 92208, F-44322 Nantes, France (c) Observatoire Oceanologique, Universite P.M. Curie, BP 44, 66651 Banyuls sur Mer, France (d) Southampton Oceanography Centre, Waterfront Campus, Empress Dock, Southampton SO14 3ZH, UK Article History: Received 7 June 2005; Revised 16 May 2006; Accepted 19 May 2006

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2006.02.001 Byline: Ricardo D. Moreno (a)(b), Jaime Palomino (a)(b), Gerald Schatten (c) Keywords: Spermatid; Spermatogenesis; Cytoskeleton; Spermatozoa; Differentiation; Acrosome; Microtubules; Golgin-97 Abstract: The acrosome is a secretory vesicle attached to the nucleus of the sperm. Our hypothesis is that microtubules participate in the membrane traffic between the Golgi apparatus and acrosome during the first steps of spermatid differentiation. In this work, we show that nocodazole-induced microtubule depolarization triggers the formation of vesicles of the acrosomal membrane, without detaching the acrosome from the nuclear envelope. Nocodazole also induced fragmentation of the Golgi apparatus as determined by antibodies against giantin, golgin-97 and GM130, and electron microscopy. Conversely, neither the acrosome nor the Golgi apparatus underwent fragmentation in elongating spermatids (acrosome- and maturation-phase). The microtubule network of round spermatids of azh/azh mice also became disorganized. Disorganization correlated with fragmentation of the acrosome and the Golgi apparatus, as evaluated by domain-specific markers. Elongating spermatids (acrosome and maturation-phase) of azh/azh mice also had alterations in microtubule organization, acrosome, and Golgi apparatus. Finally, the spermatozoa of azh/azh mice displayed aberrant localization of the acrosomal protein sp56 in both the post-acrosomal and flagellum domains. Our results suggest that microtubules participate in the formation and/or maintenance of the structure of the acrosome and the Golgi apparatus and that the organization of the microtubules in round spermatids is key to sorting acrosomal proteins to the proper organelle. Author Affiliation: (a) Unit of Reproduction and Developmental Biology, Physiology Department, Faculty of Biological Sciences, Pontifical Catholic University of Chile, Portugal 49-Santiago 340-213, Chile (b) Millennium Nucleus in Developmental Biology, Pittsburgh, PA 15213, USA (c) Pittsburgh Development Center of Magee-Womens Research Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA Article History: Received 3 August 2005; Revised 31 January 2006; Accepted 2 February 2006

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.dsr.2005.09.011 Byline: M.J.R. Fasham (a), K.J. Flynn (b), P. Pondaven (c), T.R. Anderson (a), P.W. Boyd (d) Keywords: Ecosystem model; Iron limitation; Diatom growth; Carbon budgets; Nutrient cycles; Export flux; Southern Ocean, Kerguelen islands time-series station; Southern Ocean, SOIREE site; North Atlantic, Biotrans station Abstract: A new mixed layer multi-nutrient ecosystem model, incorporating diatoms, non-diatoms and zooplankton, is described that models the role of iron in marine biogeochemical cycles. The internal cell biochemistry of the phytoplankton is modelled using the mechanistic model of Flynn [2001. A mechanistic model for describing dynamic multi-nutrient, light, temperature interactions in phytoplankton. Journal of Plankton Research 23, 977-997] in which the internal cell concentrations of chlorophyll, nitrogen, silica, and iron are all dynamic variables that respond to external nutrient concentrations and light levels. Iron stress in phytoplankton feeds back into chlorophyll synthesis and changes in photosynthetic unit (PSU) size, thereby reducing their growth rate. Because diatom silicon metabolism is inextricably linked with cell division, diatom population density (cellm.sup.-3) is modelled as well as C biomass. An optimisation technique was used to fit the model to three time-series datasets at Biotrans (47[degrees]N, 20[degrees]W) and Kerfix (50[degrees]40'S, 68[degrees]25'E) and the observations for the Southern Ocean Iron-Release Experiment (SOIREE) iron-enrichment experiment (61[degrees]S, 140[degrees]E). The model gives realistic simulations of the annual cycles of nutrients, phytoplankton, and primary production at Biotrans and Kerfix and can also accurately simulate an iron fertilisation experiment. Specifically, the model predicts the high values of diatom Si:N and Si:C ratios observed in areas where iron is a limiting factor on algal growth. In addition, the model results at Kerfix confirm previous suggestions that underwater light levels have a more limiting effect on phytoplankton growth than iron supply. The model is also used to calculate C budgets and C and Si export from the mixed layer. The implications of these results for developing biogeochemical models incorporating the role of iron are discussed. Author Affiliation: (a) National Oceanography Centre, University of Southampton, Waterfront Campus, Empress Dock, Southampton SO14 3ZH, UK (b) Wallace Building, University of Wales Swansea, SA2 8PP, UK (c) Laboratoire des Sciences de l'Environnement Marin UMR CNRS 6539, Institut Universitaire Europeen de la Mer TechnopA[acute accent]le Brest-Iroise, Place Nicolas Copernic, 29280 Plouzane, France (d) NIWA Centre of Chemical and Physical Oceanography, Department of Chemistry, University of Otago, New Zealand Article History: Received 16 August 2004; Revised 29 September 2005; Accepted 29 September 2005

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2005.09.026 Byline: Natalia Sanchez-Soriano (a), Wolfgang Bottenberg (a), Andre Fiala (b), Ulrike Haessler (a), Afroditi Kerassoviti (d), Elisabeth Knust (d), Robert Lohr (c), Andreas Prokop (a) Keywords: Dendrite; Compartmentalisation; Mosaic analysis; Cytoskeleton; Transmitter receptors; Drosophila Abstract: Dendrites represent arborising neurites in both vertebrates and invertebrates. However, in vertebrates, dendrites develop on neuronal cell bodies, whereas in higher invertebrates, they arise from very different neuronal structures, the primary neurites, which also form the axons. Is this anatomical difference paralleled by principal developmental and/or physiological differences? We address this question by focussing on one cellular model, motorneurons of Drosophila and characterise the compartmentalisation of these cells. We find that motorneuronal dendrites of Drosophila share with typical vertebrate dendrites that they lack presynaptic but harbour postsynaptic proteins, display calcium elevation upon excitation, have distinct cytoskeletal features, develop later than axons and are preceded by restricted localisation of Par6-complex proteins. Furthermore, we demonstrate in situ and culture that Drosophila dendrites can be shifted from the primary neurite to their soma, i.e. into vertebrate-like positions. Integrating these different lines of argumentation, we propose that dendrites in vertebrates and higher invertebrates have a common origin, and differences in dendrite location can be explained through translocation of neuronal cell bodies introduced during the evolutionary process by which arthropods and vertebrates diverged from a common urbilaterian ancestor. Implications of these findings for studies of dendrite development, neuronal polarity, transport and evolution are discussed. Author Affiliation: (a) Faculty of Life Sciences, WTCCMR, The University of Manchester, Oxford Road, Manchester M13 9PT, UK (b) Theodor-Boveri-Institute, Department of Genetics and Neurobiology, University of Wurzburg, Am Hubland, D-97074 Wurzburg, Germany (c) Institute of Genetics, University of Mainz, J.-J.-Becherweg 32, D-55128 Mainz, Germany (d) Institute of Genetics, University of Dusseldorf, Universitatsstr. 1, D-40225 Dusseldorf, Germany Article History: Received 4 July 2005; Revised 1 September 2005; Accepted 9 September 2005