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Anne-Calof-CV.Pdf CURRICULUM VITAE - ANNE LEIGHTON CALOF (SERVICE AND RECENT GRANT ACTIVITY HIGHLIGHTED IN BLUE) ADDRESS Department of Anatomy & Neurobiology Developmental & Cell Biology, and the Center for Complex Biological Systems University of California, School of Medicine Irvine, California 92697-1275 [email protected] EDUCATION AND PROFESSIONAL EXPERIENCE 1978 B.A. in Biology/Psychology Reed College Portland, OR 1985 Ph.D. in Neurobiology (L.F. Reichardt, Mentor) Department of Physiology University of California, San Francisco School of Medicine San Francisco, CA 1985-1987 Postdoctoral Associate (T. Jessell, Mentor) Howard Hughes Medical Institute, Center for Neurobiology and Behavior Columbia University College of Physicians & Surgeons New York, NY 1987 Assistant Instructor Molecular Embryology of the Mouse course Cold Spring Harbor Laboratory Cold Spring Harbor, NY 1987-1990 Postdoctoral Research Associate/Instructor (D. Chikaraishi, Mentor) Tufts Univ. Sch. Med., Boston, MA 1991-1995 Assistant Professor Department of Biological Sciences University of Iowa, Iowa City, IA 1995-present Assistant, Associate, Full Professor (Step VI as of July 2018) Department of Anatomy & Neurobiology, University of California, Irvine, School of Medicine 2018-present Adjunct Professor Neurobiology and Cognitive Science Center National Taiwan University, Taipei, Taiwan 1 FELLOWSHIPS, HONORS, AWARDS 1978 Phi Beta Kappa, Reed College Chapter 1978-1981 Graduate Fellowship National Science Foundation 1981-1982 Graduate Opportunity Fellowship University of California 1988 Postdoctoral Fellowship Muscular Dystrophy Association 1989-1990 Postdoctoral Fellowship National Institutes of Health NRSA 1993-1996 Basil O'Connor Starter Scholar Research Award March of Dimes Birth Defects Foundation 2003-2004 Excellence in Teaching University of California, Irvine, School of Medicine 2005-2006 Excellence in Teaching University of California, Irvine, School of Medicine 2006-2007 Excellence in Teaching University of California, Irvine, School of Medicine 2008-2009 Faculty Mentor Award to Promote Diversity Office of Graduate Studies University of California, Irvine 2008-2013 Co-Director, Cornelia de Lange Foundation Center of Excellence in Research, CdLS Foundation USA 2009-2010 Excellence in Teaching for Best First Year Course Histology for MSIs, Anne L. Calof, Course Director University of California, Irvine, School of Medicine 2012-2013 Excellence in Teaching University of California, Irvine, School of Medicine 2013-2018 Co-Director, Cornelia de Lange Foundation Center of Excellence in Research, CdLS Foundation USA 2014-2015 Excellence in Teaching University of California, Irvine, School of Medicine 2015-2016 Excellence in Teaching University of California, Irvine, School of Medicine 2016 RARE Champion of Hope in Science Award, Global Genes Alliance in Rare Diseases 2018 Excellence in Teaching Award University of California, Irvine, School of Medicine 2 STATEMENT OF RESEARCH INTERESTS AND CONTRIBUTIONS TO SCIENCE The overall goal of my laboratory’s research is to understand how changes in cell lineage progression parameters and in the expression of diverse genes act in concert to direct normal development and, when development goes awry, to cause syndromic and non-syndromic birth defects. We are particularly interested in the nervous system, but we also study other systems such as heart, limb, visceral organs, and craniofacial structures. In many of our studies, we use mouse and zebrafish models of Nipbl-deficiency (the major cause of Cornelia de Lange Syndrome (CdLS)) as systems with which to understand this question – a question that is common to many ”transcriptomopathies” that are characterized by global dysregulation of gene expression arising as a consequence of an initial genetic lesion (e.g. NIPBL haploinsufficiency in CdLS, trisomy in Down Syndrome, MECP2 mutation in Rett Syndrome, etc.). Our goals are (1) to gain insight into general principles of developmental regulation by studying animal models of Nipbl-deficiency, and (2) to use these model systems to test therapeutic interventions for CdLS. Our studies on CdLS involve, in addition to me and the members of my laboratory, other investigators at UCI and around the world. Our colleagues at UCI include Arthur Lander, Thomas Schilling (who oversees the work on zebrafish that we pursue as part of our studies of CdLS), and Kyoko Yokomori (whose primary interest in CdLS is in chromatin structure and regulation of gene expression). The papers resulting from such studies are published collaboratively, with between two and four PIs and different members of the various laboratories taking authorships, as appropriate for a given study. My lab’s most recent studies of Nipbl-deficient mice have led to novel insights into the determinants of risk for the development of congenital heart disease (see Santos et al., 2016, PLoS Biology; and review by Gelb BD (The Hole and the Whole: Lessons from Manipulation of Nipbl Deficiency. PLoS Biol. 2016 Sep 8;14(9):e2000494. doi:0.1371/journal.pbio.2000494). In addition to molecular approaches to studying development and congenital disease, I have increasingly employed a systems biology approach in my laboratory’s studies. I serve as a Theme Leader in Control of Growth and Morphogenesis at UCI’s Center for Complex Biological Systems, a NIGMS-sponsored National Center for Systems Biology. In this capacity, I work with many investigators on interdisciplinary research projects that integrate computational modeling, genomics, and high-throughput data gathering integrated with experimental developmental biology and genetics. My lab’s research in this area has mainly been focused on understanding how signaling systems participate in feedback regulation of stem and progenitor cells and the effects of such feedback on morphogenesis, patterning, and regulated growth of different tissues. The systems for which our contributions have been most significant are the olfactory epithelium, neural retina, and gustatory epithelium of the tongue, although we currently have a project to study neocortex as well. During the review period, we have published a number of studies that combine wet-bench experimentation with extensive mathematical analysis and computational modeling, as well as some papers that are purely theoretical. These studies are published collaboratively, with multiple PIs and members of the participating research groups taking authorships as appropriate for a given study. Our most recent work, published in 2016 in PLoS Computational Biology, is a theoretical exploration of the ways in which feedback effects on stem cell self-renewal can serve as a driving force in morphogenesis (Kunche et al., 2016, PLoS Computational Biology). I consider my major contributions to science to be in the following areas: 1. Vertebrate animal models to understand the origins of sporadic and syndromic birth defects: Cornelia de Lange Syndrome (CdLS) is a multi-system birth defects syndrome caused, in most cases, by haploinsufficiency for NIPBL, which encodes a cohesin regulatory protein. We helped identify NIPBL as the causative gene in most cases of CdLS, and developed the first mouse and zebrafish 3 models for Nipbl-deficiency. Our studies of these model systems led to the understanding that birth defects observed in CdLS can be attributed to global transcriptional dysregulation in Nipbl-deficient tissues. Since birth defects that arise in CdLS are also common in the general population, these models are helping us understand the etiology of sporadic birth defects, and in particular have recently contributed to our understanding of the complexity of risk determinants for congenital heart defects. Representative publications are: Krantz et al., 2004 (Nature Medicine); Kawauchi et al., 2009 (PLoS Genetics); Muto et al., 2011 (PLoS Biology); Muto et al., 2014 (PLoS Genetics); Santos et al., 2016 (PLoS Biology). 2. Understanding how neural stem cells are regulated by secreted signaling molecules: What signals govern the behavior of neural stem cells, their differentiation into committed progenitors and, subsequently, into terminally-differentiated neurons? Do different signaling molecules oppose one another in regulating progression of cells through neural lineages? What are the mechanisms by which these signals act? Do cells within a lineage contribute to building their own niche, and if so, how? The systems for which our contributions have been most significant in addressing these questions are the olfactory epithelium, neural retina, and gustatory epithelium of the tongue. Representative publications are: DeHamer et al., 1994 (Neuron); Shou et al., 1999 (Nature Neuroscience); Wu et al., 2003 (Neuron); Kim et al., 2005 (Science); Kawauchi et al., 2005 (Development); Beites et al., 2009 (Development); Kawauchi et al., 2009 (Development); Gokoffski et al., 2011 (Development). 3. Feedback and the regulation of proliferative control and spatial patterning: How do neural stem and progenitor cells know when to stop dividing and differentiate? Does feedback play a role? Can mathematical models help us understand how feedback might achieve growth control? Evidence from studies of induced neurogenesis and regeneration of the olfactory epithelium suggested to us that differentiated neurons provide negative feedback signals that regulate proliferation and size control. We identified, for the first time, a signaling molecule mediating negative feedback of neurogenesis (GDF11). We discovered that negative feedback is
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