|Dr. Mark Roberson, Professor and Chair, Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca. Dr. Roberson received his PhD at the University of Nebraska in 1990 and then completed 5 years of postdoctoral research with Richard Maurer at the University of Iowa College of Medicine and Oregon Health Sciences University in the area of molecular endocrinology of the hypothalamic-pituitary axis. Dr. Roberson joined the faculty at Cornell University in 1995 and was promoted to Associate Professor with indefinite tenure in 2001 and to full Professor in 2007. He assumed the role of Chair of the Department of Biomedical Sciences in 2007. Dr. Roberson has published extensively and has served on NIH Study Sections, as well as on the Editorial Boards of Molecular Endocrinology and Endocrinology. He is the PI on the Reproductive Sciences and Genomics Training Grant, awarded by the NICHD in 2007. Research in the Roberson lab focuses on the intracellular signal transduction cascades induced by GnRH and the mechanisms of gene activation that result from these signaling pathways. The most recent studies in the Roberson lab make use of a novel pituitary-and oocyte-specific ERK1/ERK2 conditional knock out mouse model. The Roberson lab has also recently unraveled the proteome associated with the GnRH receptor that resides in discrete compartments associated with membrane rafts. These studies reveal a unique role for β-catenin and actin signaling from within the raft. The Roberson lab also examines the molecular mechanisms for placental-specific expression, focusing on the role of the transcription factor Distal-less 3 (Dlx3) on placental trophoblast commitment and placental morphogenesis. A key Dlx3 target gene is placental growth factor, a biomarker for pre-eclampsia. Loss of Dlx3 is associated with elevated placental oxidative stress and failed expansion of fetal vasculature leading to intrauterine growth retardation.|
|Dr. Robin Davisson, Professor, Department of Biomedical Sciences, College of Veterinary Medicine and Department of Cell and Developmental Biology, Weill Cornell Medical College, Cornell University. Dr. Davisson joined the Cornell College of Veterinary Medicine in 2006, after eight years on the faculty at the University of Iowa. Her research focuses on the basic mechanisms of function, control and signaling in the cardiovascular system in health and disease, with an emphasis on cutting-edge technologies that take advantage of the functional genomics offered by murine models of cardiovascular disease. More recently she has established strong and highly informative mouse models for pre-eclampsia, the major cause of fetal and maternal mortality worldwide. She has published numerous original research and review articles and book chapters, and has been funded by multiple competitive grants from the National Institutes of Health, the American Heart Association and private industry. In addition, her cutting-edge research has earned multiple awards, including the Harry Goldblatt Award in Cardiovascular Research from the American Heart Association and the Henry Pickering Bowditch Award from the American Physiological Society. Dr. Davisson has served on several editorial boards, as well as a number of federal and private grant review panels.|
|Dr. Mariana Wolfner, PhD, Professor, Department of Molecular Biology and Genetics, College of Arts and Sciences, Cornell University. Dr. Wolfner joined the Cornell University faculty in 1983 and has been a prominent figure in the field of Drosophila genetics throughout this time. Her research is focused on understanding, at the molecular/gene level, the important reproductive processes that occur around the time when a sperm fertilizes an egg. Using the Drosophila model, the Wolfner laboratory studies the molecular signals that "activate" an oocyte to initiate embryo development and also the actions of seminal proteins that female flies receive from the males with which they mate. She has published over 130 papers in peer-reviewed journals and has served on a number of NIH study sections, including current membership on CMIR. She is on the Editorial Boards of several journals, including Genetics and Molecular Reproduction and Development, and she is or has been an Officer of the Genetics Society of America and the AAAS. She has been given numerous honors for her research endeavors, including a Junior Faculty Research Award from the American Cancer Society, a Career Advancement Award from the National Science Foundation, a Lady Davis Fellowship, and election as a Fellow of the American Association for the Advancement of Science.|
A new study from Andrew Grimson's lab, in collaboration with Paula Cohen's lab, has identified a key pathway required for maintenance of sex chromosome telomere integrity. Using conditional knockout mice for Dicer and Dgcr8, two key enzymes required for small RNA processing, Modzelewski et al (2015) show that loss of small RNAs during prophase I leads to telomere fusion events specifically involving the X and Y chromosomes. For further information, see the May edition of Journal of Cell Science
A recent publication by Dabaja et al (2015) has identified key cell:cell interactions that are necessary to establish normal profiles of one key microRNA, miR202-5p, in Sertoli cells. This is the first example of a germ cell regulatory interaction that is necessary for miR expression in neighboring somatic cells of the testis
The lab of Center member John Schimenti recently identified the DNA damage checkpoint pathway responsible for culling oocytes that fail to repair double stranded breaks (DSBs) that occur during meiosis or which arise in a female's oocyte pool (Bolcun-Filas et al, Science 343:533-536, 2014). Using combinations of mutants involved in recombination and DNA damage responses, they found that this pathway involves signaling of checkpoint kinase 2 (CHK2) to both p53 and p63. Disruption of this checkpoint pathway restored fertility to females that normally would be deficient of all oocytes due to defects in meiotic recombination or exposure to radiation. This discovery opens the way to using available CHK2 inhibitors to protect the oocytes of women undergoing cancer therapy that would normally cause infertility.