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 b-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.
For more information about Dr. Roberson's research, please see his lab website.
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.