A Scientist Emeritus is a special designation that can be given to distinguished scientists who wish to retire but still maintain an ongoing working relationship at NIH. The following are appointed Scientist Emeritus by NICHD’s Division of Intramural Research.
Greti Aguilera, M.D. had a distinguished career at the NICHD, lasting for over 35 years, studying adrenal steroidogenesis and neuroendocrine mechanisms of adaptation to stress.
Dr. Aguilera received her M.D. from the University of Chile in 1968. After graduation, she was awarded a prestigious fellowship to join a clinical/basic research post-graduate program at the University of Chile, in which she received training in clinical and basic endocrinology, later serving as Associate Professor at the Department of Physiology. In 1975, Dr. Aguilera joined the laboratory of Dr. Kevin Catt at NICHD, first as an International Fogarty fellow and then as a Visiting Scientist. In 1984, Dr. Aguilera was appointed as Senior Investigator in NICHD, and in 1989, as Chief of the Section of Endocrine Physiology, a position she held until her retirement in 2014.
Dr. Aguilera’s research sought to establish a basic understanding of the neuroendocrine mechanisms underlying homeostatic regulation during stress with emphasis on the regulation of the components of the hypothalamic pituitary adrenal axis, neurohypophyseal and autonomic systems. Over the years her laboratory made important contributions to the current knowledge on the regulation and the relative roles of corticotropin releasing hormone (CRH) and vasopressin on the HPA axis, and characterization of the properties, signaling-transduction and regulation of the receptors and actions for these peptide hormones. In addition, to determining the role of vasopressin on the stress response, the work identified novel effects of vasopressin as a neuroprotective agent and trophic factor for the pituitary corticotroph. Her most recent work demonstrating that activation of CRH transcription requires the CREB coactivator, Transducer of Regulated CREB activity (TORC), regulated by the protein kinase, salt inducible kinase (SIK), uncovered a missing link in current knowledge of the regulation of CRH transcription. In keeping with the importance of a cyclic AMP responsive element (CRE) in the CRH promoter in the regulation of CRH transcription, Dr. Aguilera and her colleagues demonstrated that HPA axis hyperactivity following early life stress is associated with increased CRH transcription in response to stress, and hypomethylation CRH promoter CRE. In addition, research addressing the mechanisms of pulsatility of glucocorticoid secretion recently demonstrated that each ACTH-induced secretory pulse is associated with induction of steroidogenic proteins transcription.
Dr. Aguilera's contributions to the knowledge of the physiological, cellular and molecular aspects of the neuroendocrine mechanisms of stress adaptation throughout the years have had profound impact in the field. In 2007, she received the Mortyn Jones Memorial Medal from the British Society of Neuroendocrinology in recognition of her contributions.
Igor Dawid, Ph.D., headed the Section on Developmental Biology, NICHD from 1982 until his retirement in December 2016. He also served as chief of the Laboratory of Molecular Genetics from 1982-2010, head of the Program in Genomics of Differentiation from 2007-2010, and acting scientific director of NICHD from 1998-2000.
Dr. Dawid received his Ph.D. from the University of Vienna and completed his postdoctoral training at the Massachusetts Institute of Technology before taking a position with the Carnegie Institution of Washington in Baltimore, Maryland, in the Department of Embryology. He arrived at NIH in 1978, working first with the National Cancer Institute before moving to NICHD in 1982.
In his career spanning more than five decades, Dr. Dawid studied molecular mechanisms of development, primarily using the frog Xenopus laevis and the zebrafish Danio rerio as model systems. During this time, he made several contributions to the field including obtaining molecular evidence for the maternal inheritance of mitochondrial DNA in animals, co-discovering amplification of ribosomal genes in frog oocytes, being a leader in the study of differential gene expression in embryogenesis, illuminating the role of Lhx genes and the Wnt pathway in axis determination, and contributing to the elucidation of additional pathway in the regulation of vertebrate development.
Recent work in his lab included studies on (i) the role of Kctd15 in regulating neural crest formation; (ii) molecular interactions of Kctd15 and transcription factor AP-2; (iii) the generation of mutations in Kctd15 genes and characterization of their phenotypes; (iv) the biological role of the Lnx family of E3 ubiquitin ligases; and, (v) the regulation of the Notch pathway through control of protein stability in pancreas formation in the zebrafish embryo.
Dr. Dawid has authored more than 290 publications. For his achievements, he has been honored with membership in the National Academy of Sciences and the American Academy of Arts and Sciences, the Lifetime Achievement Award of the Society for Developmental Biology, and honorary doctoral degrees from Lausanne University, Switzerland and the Technion, Israel.
David C. Klein, Ph.D., has made seminal contributions to the fields of chronobiology and neuroendocrinology through work on the pineal gland.
Dr. Klein received his B.A. from Cornell University and his Ph.D. from Rice University, where he studied the role of calcitonin in bone metabolism under Roy Talmage. During postdoctoral work at the University of Rochester with Larry Raisz, he discovered that prostaglandins promote bone resorption, which has had broad clinical impact. While at Rochester, he initiated independent work on the pineal gland. This research continued after joining NICHD in 1969 and grew into one of the leading research programs devoted to the pineal gland.
During his career, Dr. Klein established productive collaborations with experts in a broad range of disciplines including functional neuoanatomy, molecular biology, pharmacology, electrophysiology, histology, and structural biology. The advances resulting from these collaborations enriched and invigorated the field of pineal research. Specific advances include contributions to understanding the role of the suprachiasmatic nucleus as “The Mind’s Clock” in controlling circadian rhythms; a detailed description of the mechanisms involved in regulating melatonin production focused on arylalkylamine N-acetyltransferase; the role of 14-3-3 proteins as functional regulators, studies on daily changes in the pineal transcriptome; and a theory explaining the evolution of the pineal gland and retina from a common photodetector.
Dr. Klein was appointed Scientist Emeritus in 2015 and continues to participate in research through an international network of scientists. He is currently investigating melatonin-related signaling; pinealocyte heterogeneity using single-cell RNA sequencing; circadian system organization; neural regulation of RNA isoforms; and 24-hour dynamics in the transcriptomes of the pineal gland, retina, suprachiasmatic nucleus and other tissues. Dr. Klein has contributed over 400 publications to the biomedical literature.
Judith G. Levin, Ph.D., was formerly Head of the Section on Viral Gene Regulation in the Program in Genomics of Differentiation (now the Division of Developmental Biology) at NICHD.
Dr. Levin received her B.A. in Chemistry from Barnard College, her M.A. in Biochemistry from Harvard University, and her Ph.D. in Biochemistry from Columbia University. She spent her entire professional career at the NIH, coming initially to work as a postdoctoral fellow in the laboratory of Dr. Marshall Nirenberg, where she performed studies on protein synthesis and the genetic code.
Since the 1970s, Dr. Levin has been investigating the molecular mechanisms involved in retrovirus replication. In her early work, she studied murine leukemia virus (MLV) replication and made several novel discoveries: (i) MLV assembly proceeds in the absence of genomic RNA, although virions contain the full complement of viral proteins; (ii) MLV-infected cells contain two non-equilibrating pools of full-length viral RNA, one for encapsidation (short-lived) and the other functioning as the mRNA for the Gag precursor (long-lived), which rationalizes the earlier observation; and (iii) A series of papers defining the unique mechanism for MLV translational read-through suppression, which is required for synthesis of the Pol proteins, protease, reverse transcriptase, and integrase.
The broad objective of Dr. Levin’s recent research has been to expand knowledge of HIV replication strategies and host defense mechanisms, and thereby contribute to the development of new treatments for HIV/AIDS patients. She has studied the effects of mutations in structural elements of the HIV-1 capsid protein on infectivity, viral core architecture, and reverse transcription. She also has had a long-standing interest and leadership role in research on the HIV-1 nucleocapsid protein (NC) and has made numerous contributions regarding the critical importance of NC function for specific and efficient reverse transcription. Her reviews on the nucleic acid chaperone activity of NC (i.e., the ability of NC to remodel nucleic acid structures to form the most thermodynamically stable conformations) continue to be cited widely in the retrovirus literature.
More recently, Dr. Levin has undertaken studies of the human APOBEC3 (A3) proteins, a family of seven cellular cytidine deaminases, which function as DNA mutators and restrict HIV-1 and other pathogens. Her laboratory was one of the first to report biochemical studies of highly purified, catalytically active A3G. This work led to the proposal of a “roadblock” effect of A3G on reverse transcription, indicating that HIV-1 restriction can occur by deaminase-independent as well as by deaminase-dependent mechanisms. In other studies, Dr. Levin’s group has utilized a multi-disciplinary approach, targeting the molecular properties of A3A, A3H, and A3B (C-terminal catalytic domain) and their relation to biological activity and three-dimensional protein structure.
Mark Mayer, Ph.D., was appointed Scientist Emeritus in 2016, following a distinguished career in the NICHD lasting more than 34 years. During that time, he made prolific contributions to our understanding of the molecular mechanisms of neurotransmitter receptor function, with a special focus on AMPA, kainate and NMDA receptors, the major mediators of excitatory synaptic transmission in the vertebrate brain.
Dr. Mayer received a B.Sc. 1st class hons degree in Pharmacology from the University of Bristol in 1987. He obtained his Ph.D. from the University of London in 1980 and immediately moved to the United States as a Harkness Fellow of the Commonwealth Fund of New York. In 1981, he spent a year in the Laboratory of Developmental Biology (LDN), NICHD where his career in ion channel biophysics took root. After returning to the U.K., where he won a Beit Memorial Fellowship, he maintained close contacts with the NIH, and during the summer of 1983 spent four months in LDN where he did seminal experiments that defined the voltage dependent block of NMDA receptors by Mg2+. Dr. Mayer returned to LDN as a visiting associate in 1984, where he made another important discovery, defining the high Ca2+ permeability of NMDA receptors.
In 1987, Dr. Mayer was appointed head of the Unit of Neurophysiology and Biophysics at NICHD, where he established a research program that would continue to define the function of glutamate receptor ion channels. Dr. Mayer won the Society for Neuroscience young investigator award in 1989 and was tenured in 1991. In 1993, Dr. Mayer established the Laboratory of Cellular and Molecular Neurophysiology in NICHD, and was appointed under the Senior Biomedical Research Service in 1998. With the goal of using structural methods to study glutamate receptor function, Dr. Mayer took a year-long sabbatical leave in October 1999 to study biochemistry and X-ray crystallography in Eric Gouaux's laboratory at Columbia University. Upon returning to NIH, Dr. Mayer reorganized his research group, and continued to do important work combining high resolution ion channel biophysics with X-ray diffraction to reveal molecular mechanisms for the subtype specific ligand binding profiles of AMPA, kainate and NMDA receptors; the role of ligand binding domains in AMPA and kainate receptor desensitization; and the identification of allosteric ion binding sites in kainate receptors. His most recent work, in collaboration with Sriram Subramaniam's group at the National Cancer Institute, used single particle cryo-EM to reveal the conformational gating cycle underlying glutamate receptor activation and desensitization.
Dr. Mayer spent his career at the NIH studying the molecular mechanisms underpinning the function and structure of glutamate receptor ion channels, having made multiple crucial discoveries over more than three decades of research. He has published more than 120 peer reviewed research papers and multiple influential reviews.
Owen M. Rennert, M.D. was the Head of the Laboratory of Clinical and Developmental Genomics from 2009 to 2013 and served as Scientific Director of the Division of Intramural Research NICHD from 2000 to 2009.
Dr. Rennert obtained his M.D. from the University of Chicago, School of Medicine in 1961. Thereafter, he did a year of pediatric residency (1961-62) at the University of Chicago, postdoctoral fellow in Biochemistry (1962-62), and a second year of pediatric residency at the University of Chicago (1963-64). He obtained his M.S. in Biochemistry in 1963, also from the University of Chicago. Upon completion, he became a research/clinical fellow at the National Institute of Neurological Disorders and Stroke from 1964-66. Dr. Rennert then pursued a fulfilling and accomplished academic career. From 1998-2000 he was appointed special Advisor to the Director of NICHD, and subsequently Scientific Director of NICHD from 2000-2009, and head of the Lab of Clinical and Developmental Genomics. In 2009, he stepped down as Scientific Director to returned full-time to his research.
Dr. Rennert's scientific career spans more than half a century and traverses both basic and clinical research. He contributed significantly to the early development of biochemical genetics and was a pioneer researcher in this field; in particular, the mucopolysaccharidosis and glycogen storage diseases and inborn metabolic disorders of copper. His laboratory is responsible for the discovery of deranged copper metabolism in cultured skin fibroblasts derived from patients of Wilson's disease and Menke's disease and offered an in vitro platform for diagnosis as well as for understanding the molecular genetics of these disorders. He later focused on the molecular genetics of endocrine disorders, in particular disorders caused by mutations of the luteinizing hormone receptor. His laboratory group reported more than 60% of all know activating mutations of this receptor and established itself as the core laboratory in the US for the diagnosis of familial male-limited precocious puberty, a disorder resulted from these mutations. Dr. Rennert is among the pioneers of polyamine research. His earlier work established polyamines as a group of small cationic molecules that play critical roles in biological processes in health and diseases and his studies laid a solid foundation for a field which is still being actively researched. He investigated the basic biology and pathophysiology of a number of diseases including cystic fibrosis and collagen disorders. At the NIH, he started mapping the developmental genomics of male gonads and differentiating germ cells, and established several sequence-based databases, including that of male gonad, human male germ cells, and long non-coding RN As, all of which are accessible by the public. In more recent years, his laboratory took on the task of investigating the pathophysiology of autism spectrum disorders and the molecular biology of the autistic brain. His laboratory also developed induced pluripotent stem cell models for a number of inherited disorders, including a selected subgroup of autism spectrum disorders.
Heinrich Westphal, M.D., was formerly Head of the Section on Mammalian Molecular Genetics in what was then the Program in Genomics of Differentiation at the NICHD.
Dr. Westphal received his M.D. in 1960 in his native Germany. He then completed his postdoctoral work at Salk Institute in San Diego, CA under Dr. Renato Dulbecco where he was able to detect viral genes, later named oncogenes, in cells that gained cancerous growth properties as a result of exposure to small DNA tumor viruses. After spending two years as independent researcher at Cold Strong Harbor Tumor Virus Laboratory under Dr. James D. Watson, Dr. Westphal joined NICHD in 1972, where he spent the remainder of his career.
Dr. Westphal's first experiments at NICHD were directed toward studying complexes of tumor virus messenger RNA and DNA in the electron microscope. His research team was one of three groups to report the first exciting electron micrographs signaling the phenomenon of RNA splicing. Dr. Westphal received the U.S. Senior Scientist Award of the Humboldt Foundation in recognition of this work.
In subsequent years Dr. Westphal's studies on the molecular genetics of cancer shifted from cell cultures to the living organism. His laboratory became one of the first worldwide to master the technique of generating strains of gene-altered mice. Work was initially focused on the very beginnings of cancer in the initial tumor cell from which the disease spreads into the surrounding tissue. By targeting viral oncogenes to the eye lens of transgenic mice, his team was able to show that the state of cell differentiation in this tissue is inversely proportional to the ability of viral oncogenes to produce malignant and invasive tumors. Following a decade of observations on oncogenesis versus differentiation in the transgenic mouse, the laboratory established a new focus of research, the molecular genetics of development. Dr. Westphal and his group began to characterize mouse genes that govern pattern formation and organogenesis in the mouse embryo resulting in the elucidation of key genetic events governing pituitary organogenesis, gonad and kidney formation and forebrain development, as well as gene defects responsible for complex human genetic diseases, including holoprosencephaly and Hirschsprung disease. Most recently, Dr. Westphal incorporated induced pluripotent stem (iPS) cell technology in his research program in an effort to address disease mechanisms of rare childhood disorders and to create the premises of novel drug therapy including Smith-Lemli-Opitz syndrome (SLOS), an autosomal recessive disorder caused by mutations of the 7-dehydrocholesterol reductase (DHCR7) gene which impairs the final step of cholesterol synthesis.
Over his career, Dr. Westphal contributed over 260 publications to the biomedical literature and his innovation of using the Cre/lox technology as a tool for generating conditional gene mutations in the mouse has been widely adopted in the field.