Search

To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1552-6569.2008.00326.x Keywords: Cerebellum; neurodevelopment; hindbrain; neuroimaging; magnetic resonance imaging (MRI) Abstract: ABSTRACT BACKGROUND AND PURPOSE The Homeobox A1 (HOXA1) gene plays a critical role during development of the hindbrain in mice. Little is currently known about the relation between this gene and human brain development. The HOXA1 A218G polymorphism has been found to be associated with autism and larger head circumference in autistic patients. Similar effects were revealed also in healthy children but not in adult controls. The aim of this study was to investigate the role of the A218G polymorphism on the hindbrain structure of healthy adults. METHODS Healthy persons from two independent groups underwent 3-dimensional high resolution magnetic resonance (MR) exam. Group A was made of 80 persons (27 G allele carriers and 53 non-carriers) and Group B of 72 (26 carriers and 46 non-carriers). Statistical parametric mapping 2 (SPM2) were used to perform voxel-based analysis of the gray matter (GM) of the hindbrain in carriers and non. Significance threshold was set at .05 with small volume correction using a cerebellar mask. RESULTS In Group A, G carriers exhibited decreased GM volume in the superior posterior and anterior lobe of the cerebellum bilaterally. In Group B, decreased GM volume were found across the entire left cerebellar cortex. CONCLUSIONS These data suggest that the HOXA1 A218G polymorphism may affect cerebellar development in humans. Author Affiliation: (1)From the LENITEM Laboratory of Epidemiology, Neuroimaging, and Telemedicin-IRCCS Centro S. Giovanni di Dio-FBF, Brescia, Italy (EC, MB, CT, GBF); NeuroBioGen Lab-Memory Clinic-IRCCS Centro S. Giovanni di Dio-FBF, Brescia, Italy (RG, LB, GB); Robert Giffard Laval University Research Center, Quebec City, Canada (SD); Radiology Department, Faculty of Medicine, Laval University, Quebec City, Canada (SD); Psychogeriatric Ward-IRCCS Centro S. Giovanni di Dio-FBF, Brescia, Italy (GBF); Proteomics Unit-IRCCS Centro S. Giovanni di Dio-FBF, Brescia, Italy (RG).[Correction added after online publication 14-September-2009: Received date has been corrected.] Article History: Acceptance: Received December 21, 2007, and in revised from August 12, 2008. Accepted for publication September 15, 2008. Article note: Correspondence: Address correspondence to Giovanni B Frisoni, LENITEM-Laboratory of Epidemiology, Neuroimaging and Telemedicine, IRCCS San Giovanni di Dio-FBF, Via Pilastroni 4, 25125 Brescia, Italy, E-mail: papers@centroAlzheimer.it

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.ydbio.2009.04.030 Byline: Haruo Okado (a), Chiaki Ohtaka-Maruyama (a), Yoshinobu Sugitani (b), Yuko Fukuda (c), Reiko Ishida (c), Shinobu Hirai (a), Akiko Miwa (a), Akiyo Takahashi (a), Katsunori Aoki (d), Keiji Mochida (e), Osamu Suzuki (f), Takao Honda (g), Kazunori Nakajima (g), Masaharu Ogawa (b), Toshio Terashima (h), Junichiro Matsuda (f), Hitoshi Kawano (i), Masataka Kasai (c) Keywords: RP58; Transcriptional repressor; Cerebral cortex; Apoptosis; Cell-cycle exit; Progenitor cell Abstract: The neocortex and the hippocampus comprise several specific layers containing distinct neurons that originate from progenitors at specific development times, under the control of an adequate cell-division patterning mechanism. Although many molecules are known to regulate this cell-division patterning process, its details are not well understood. Here, we show that, in the developing cerebral cortex, the RP58 transcription repressor protein was expressed both in postmitotic glutamatergic projection neurons and in their progenitor cells, but not in GABAergic interneurons. Targeted deletion of the RP58 gene led to dysplasia of the neocortex and of the hippocampus, reduction of the number of mature cortical neurons, and defects of laminar organization, which reflect abnormal neuronal migration within the cortical plate. We demonstrate an impairment of the cell-division patterning during the late embryonic stage and an enhancement of apoptosis of the postmitotic neurons in the RP58-deficient cortex. These results suggest that RP58 controls cell division of progenitor cells and regulates the survival of postmitotic cortical neurons. Author Affiliation: (a) Department of Molecular Physiology, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan (b) Ogawa research unit, Neuro-developmental disorder research group, Brain Science Institute, Riken, Saitama 351-0198, Japan (c) Department of Immunology, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan (d) Department of Hematology (Internal Medicine), The University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan (e) Bioresource Center, RIKEN, Tsukuba, Ibaraki 305-0074, Japan (f) Department of Veterinary Science, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan (g) Department of Anatomy, Keio University School of Medicine, Tokyo 160-8582, Japan (h) Division of Anatomy and Developmental Neurobiology, Department of Neuroscience, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan (i) Department of Developmental Morphology, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan Article History: Received 23 August 2008; Revised 1 April 2009; Accepted 24 April 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2008.10.014 Byline: S.J. Choi (a), G.D. Roodman (b), J.Q. Feng (c), I.S. Song (a), K. Amin (a), P.S. Hart (d), J.T. Wright (e), N. Haruyama (f), T.C. Hart (a) Keywords: Rodent; Transgenic mice; DLX3; Osteoclast; Bone mineralization; Interferon-gamma Abstract: Distal-less 3 (DLX3) gene mutations are etiologic for Tricho-Dento-Osseous syndrome. To investigate the in vivo impact of mutant DLX3 on bone development, we established transgenic (TG) mice expressing the c.571_574delGGGG DLX-3 gene mutation (MT-DLX3) driven by a mouse 2.3 Col1A1 promoter. Microcomputed tomographic analyses demonstrated markedly increased trabecular bone volume and bone mineral density in femora from TG mice. In ex vivo experiments, TG mice showed enhanced differentiation of bone marrow stromal cells to osteoblasts and increased expression levels of bone formation markers. However, TG mice did not show enhanced dynamic bone formation rates in in vivo fluorochrome double labeling experiments. Osteoclastic differentiation capacities of bone marrow monocytes were reduced in TG mice in the presence of osteoclastogenic factors and the numbers of TRAP(+) osteoclasts on distal metaphyseal trabecular bone surfaces were significantly decreased. TRACP 5b and CTX serum levels were significantly decreased in TG mice, while IFN-[gamma] levels were significantly increased. These data demonstrate that increased levels of IFN-[gamma] decrease osteoclast bone resorption activities, contributing to the enhanced trabecular bone volume and mineral density in these TG mice. These data suggest a novel role for this DLX-3 mutation in osteoclast differentiation and bone resorption. Author Affiliation: (a) Human Craniofacial Genetics Section, Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20854, USA (b) Department of Medicine, Division of Hematology-Oncology, University of Pittsburgh, Pittsburgh, PA, USA (c) Biomedical Sciences, Baylor College of Dentistry, Texas A&M Health Science Center, Dallas, TX, USA (d) Office of the Clinical Director, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA (e) Department of Pediatric Dentistry, University of North, Chapel Hill, NC, USA (f) Division of Oral Dysfunction Science, Tohoku University, Graduate School of Dentistry, Sendai, Japan Article History: Received 1 August 2008; Revised 5 September 2008; Accepted 2 October 2008

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1365-2745.2008.01452.x Byline: Olivier Honnay (1), Hans Jacquemyn (1), Kris Van Looy (2), Katrien Vandepitte (1), Peter Breyne (2) Keywords: AFLP; assignment analysis; genetic differentiation; genetic drift; plant metapopulation; plant migration and colonization; riparian plant species Abstract: Summary Metapopulation dynamics - the recurrent extinction and colonization in spatially discrete habitats - is expected to strongly affect within and between population genetic diversity. So far, however, accounts of true plant metapopulations are extremely scarce. We monitored the colonization and extinction dynamics of an assemblage of populations of the annual Erysimum cheiranthoides on stony river banks during three consecutive years. Each year, winter flooding drives some populations to extinction, while vacant banks may become colonized. We describe the dynamics of these ephemeral populations using amplified fragment length polymorphism (AFLP) markers to quantify changes in the metapopulation genetic structure over time, and assessing the direction and relative amount of migration and colonization events. Average extinction and colonization rates were high (0.39 and 0.34, respectively). While population genetic differentiation (F.sub.ST) tripled from 0.06 in 2005 to 0.17 in 2007, total metapopulation genetic diversity remained fairly constant through the years. Genetic assignment analyses allowed assigning more than 50% of the genotyped individuals to populations extant the year before. Colonizing individuals originated from different source populations (&phiv; << 1) and there was considerable evidence of upstream seed dispersal. The degree and pattern of spatial genetic structure varied between years and was related to variation in the flooding intensity of the Meuse River through the years. Possibly, activation of the soil seed bank also played a role in structuring the genetic make-up of the populations. Because migration and colonization events were qualitatively equal, and colonizing individuals originated from different sources, the increase in F.sub.ST was in agreement with previous theoretical work. Very high migration and colonization rates, and the short monitoring period, may explain why there was no loss of genetic diversity from the metapopulation through recurrent extinction and colonization events. Synthesis. This study gives one of the first accounts of the dynamics of a true plant metapopulation. Temporal monitoring of genetic variation gave evidence of extensive and bidirectional seed dispersal, highly variable and increasing genetic differentiation, and rather constant within population genetic diversity. An important suggestion from this research is to include a dormant seed stage in further theoretical work on (meta) population genetics. Author Affiliation: (1)Laboratory of Plant Ecology, Division of Plant Ecology and Systematics, University of Leuven, Arenbergpark 31, B-3001 Heverlee, Belgium; and (2)Research Institute for Nature and Forest, Kliniekstraat 25, B-1070 Brussels, Belgium Article History: Received 7 July 2008; accepted 26 September 2008Handling Editor: Joop Ouborg Article note: (*) Correspondence author. E-mail: olivier.honnay@bio.kuleuven.be

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2008.06.013 Byline: Barry R. Palmer (a), Martin D. Jarvis (a), Anna P. Pilbrow (a), Katrina L. Ellis (a), Chris. M. Frampton (a), Lorraine Skelton (a), Tim G. Yandle (a), Rob N. Doughty (b), Gillian A. Whalley (b), Chris J. Ellis (b), Richard W. Troughton (a), A. Mark Richards (a), Vicky A. Cameron (a) Abstract: Polymorphisms of the angiotensin-converting enzyme 2 (ACE2) gene, which is located on the X chromosome, have been associated with hypertension and left ventricular hypertrophy in previous studies. We tested the hypothesis that the rare allele of an ACE2 gene polymorphism was associated with risk factors for and adverse outcome after acute coronary syndrome (ACS) events. Author Affiliation: (a) Department of Medicine, Christchurch Cardioendocrine Research Group, Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch, New Zealand (b) Department of Medicine, Faculty of Medicine and Health Sciences, University of Auckland, Auckland, New Zealand Article History: Received 15 February 2008; Accepted 9 June 2008 Article Note: (footnote) Funding from a University of Otago (Dunedin, New Zealand) ORG grant, the Health Research Council of NZ (Auckland, New Zealand), the National Heart Foundation (NHF) of NZ (Auckland, New Zealand), the Maurice and Phyllis Paykel Trust (Auckland, New Zealand), and Lottery Health (Wellington, New Zealand) is acknowledged. A.P.P. held a Foundation for Research and Technology Postdoctoral Fellowship, G.A.W. a NHF Senior Fellowship, and A.M.R. the NHF Chair of Cardiovascular Studies.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2005.09.011 Byline: Jiuhong Kang (1), Yufeng Shi (1), Bin Xiang (2), Bin Qu (1), Wenjuan Su (2), Min Zhu (2), Min Zhang (1), Guobin Bao (1), Feifei Wang (2), Xiaoqing Zhang (2), Rongxi Yang (1), Fengjuan Fan (1), Xiaoqing Chen (2), Gang Pei (1), Lan Ma (2) Abstract: Chromatin modification is considered to be a fundamental mechanism of regulating gene expression to generate coordinated responses to environmental changes, however, whether it could be directly regulated by signals mediated by G protein-coupled receptors (GPCRs), the largest surface receptor family, is not known. Here, we show that stimulation of delta-opioid receptor, a member of the GPCR family, induces nuclear translocation of [beta]-arrestin 1 ([beta]arr1), which was previously known as a cytosolic regulator and scaffold of GPCR signaling. In response to receptor activation, [beta]arr1 translocates to the nucleus and is selectively enriched at specific promoters such as that of p27 and c-fos, where it facilitates the recruitment of histone acetyltransferase p300, resulting in enhanced local histone H4 acetylation and transcription of these genes. Our results reveal a novel function of [beta]arr1 as a cytoplasm-nucleus messenger in GPCR signaling and elucidate an epigenetic mechanism for direct GPCR signaling from cell membrane to the nucleus through signal-dependent histone modification. Author Affiliation: (1) Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, The Graduate School, Chinese Academy of Sciences, Shanghai 200031, China (2) Pharmacology Research Center, Shanghai Medical College, The Graduate School, Fudan University, Shanghai 200032, China Article History: Received 29 March 2005; Revised 7 July 2005; Accepted 12 September 2005 Article Note: (miscellaneous) Published: December 1, 2005

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2005.03.062 Byline: Daisaku Nakatani (a), Hiroshi Sato (a), Yasuhiko Sakata (a), Issei Shiotani (a), Kunihiro Kinjo (a), Hiroya Mizuno (a), Masahiko Shimizu (a), Hiroshi Ito (b), Yukihiro Koretsune (c), Atsushi Hirayama (d), Masatsugu Hori (a) Abstract: In patients with acute myocardial infarction (AMI), depressive symptoms increase the risk for cardiac events. Recently, the S allele of the serotonin transporter (5-HTT) gene-linked polymorphic region was shown to reduce transcription of this gene and thus reduce serotonin reuptake, and this allele is linked with depressive symptoms as well as other psychiatric diseases. However, the influence of the S allele on depressive symptoms and cardiac events after AMI is unclear. Author Affiliation: (a) Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan (b) Sakurabashi Watanabe Hospital, Osaka, Japan (c) Osaka National Hospital, Osaka, Japan (d) Osaka Police Hospital, Osaka, Japan Article History: Received 30 August 2004; Accepted 15 March 2005 Article Note: (miscellaneous) This work was supported by a grant-in-aid for University and Society Collaboration (15590743) from the Japanese Ministry of Education, Culture, Sports, Science, and Technology (Tokyo, Japan) and by a research grant from the Japan Arteriosclerosis Prevention Fund.