Two students will be selected and trained in areas of reproductive biology and developmental sciences and participate in career development workshops to prepare them for graduate school. The opportunity to attend the annual Conference of the Society for the Study of Reproduction may also be available.
This is a 10 week training program to start on May 27th, 2022. Travel, lodging and a $2,000 stipend will be provided to the selected students.
Applicants: Preferentially, juniors or rising seniors are invited to apply. The students are encouraged to select a research program of interest.
Join us in a summer full of research and career development activities and FUN!!
RDSP Su2022 DSRRP Faculty Labs
The reproductive health of managed and free-ranging wildlife is critical to the survival of threatened species. The Reproductive Health Surveillance Program collects reproductive tracts from zoo animals after neutering or death with the goal of documenting normal and abnormal reproductive anatomy in a wide variety of species as well as monitoring for emerging diseases and the effects of management and contraceptive compounds. The RHSP has an archive of over 3000 tracts from hundreds of mammalian species, including microscopic slides and genetic material from many of these animals. Projects in the past have included surveys of reproductive health in polar bears, African painted dogs, great apes, and giraffe.
Early events of mammalian pregnancy, although crucial for normal development, are poorly understood. Owing to the small size and transparent nature of the early embryo, development from fertilization to blastocyst stages has been extensively documented by imaging. On the other hand, a deeper understanding of the 3D architecture of the embryo’s uterine environment and the uterine glands has lagged behind. The Arora Lab (Arora Lab at Michigan State University) uses developmental genetics, 3D imaging, computational image analysis, and gene expression analysis, to understand how hormones influence the uterine architecture to modulate receptivity and implantation.
Cibelli’s lab focuses on understanding the reprogramming process once a somatic cell is introduced into an unfertilized oocyte. We believe that by understanding its primary mechanism, we will be able to increase the efficiency of animal cloning. As models, we use zebrafish and bovine. Nuclear Transfer-Cloning, also named Somatic Cell Nuclear transfer (SCNT) it is recognized as the boldest reprogramming approach known, where the nucleus of a differentiated cell must be reprogrammed in a matter of hours, and become a cell capable of developing into a new individual to the extreme of bypassing the complex biological processes of gametogenesis and fertilization. Embryos thus reengineered can develop into live offspring. Although remarkable, this process is still inefficient. In all species cloned, less than 3 % of reconstructed oocytes result in live births.
Studies in the Fazleabas laboratory (https://rdsp.canr.msu.edu/faculty/6-fazleabas-asgi-t-phd) has significant translational relevance related to improved pregnancy outcomes in infertile women as well as understanding the etiology and the pathophysiology associated with the development of endometriosis. A significant area of his research emphasis has been to study the early events associated with maternal-fetal interactions during the establishment of pregnancy and the mechanisms by which these interactions are affected in women and non-human primates with endometriosis. These studies focus embryo implantation and maternal fetal interactions and have focused specifically on the role of NOTCH1 during the process of decidualization. In addition to studies in the non-human primate and in stromal cells from women, his laboratory has also developed novel transgenic mouse models which have cell specific gain of function and loss of function properties to study embryo implantation, decidualization and endometriosis. In addition, the mechanisms by which inflammation enhance endometriotic lesion development by regulating cell proliferation, suppression of apoptosis and fibrosis are also under investigation.
My lab focuses on how a brief period of early life growth restriction influences cardiovascular development. Specifically, we have observed that growth-restricted mice respond negatively to an exercise intervention, which is atypical. Therefore, the current projects in the lab focus on determining mechanism by which growth-restricted mice are non-responders to exercise.
Research in the Hoffmann lab (https://www.canr.msu.edu/hoffmann/) focuses on the contribution of cell endogenous 24h rhythms, termed circadian rhythms, in fertility and pregnancy success. For the DSRRP we can offer a project focused on understanding the role of circadian rhythms in uterine function in pregnancy and labor onset. This project will require working with tissues from mice, and an interest in learning about circadian rhythms, uterine function, pharmacological studies, and molecular biology. The goal of the project is to elucidate why time of day impacts the capacity of the oxytocin receptor to regulate uterine contractions. These studies will be a first step towards understanding why labor induction, which is typically done using oxytocin (Pitocin), often is unsuccessful. We hypothesize that the time of day of labor induction should be aligned with the time of day where oxytocin receptor more efficiently promotes uterine contractions.
The Latham laboratory studies mechanisms regulating oogenesis and early embryogenesis with an emphasis on using genetic mouse genetic models and the bovine model. Studies are address the regulation of maternal mRNA regulation in oocytes and embryos, chromatin regulation in the embryo, and mechanisms whereby maternal health impact oocyte quality. Recent studies have incorporated transcriptome analysis by RNA sequencing followed by pathway analysis, as well as cross-species comparisons to better understand shared and species-specific aspects.
The initial germ cell population, known as primordial germ cells (PGCs), arises from proximal epiblast around embryonic day 7 in mice. These PGCs subsequently migrate to the genital ridge. In male, PGCs become spermatogonia and eventually develop into sperm after birth. Disrupting this process causes male infertility. My main research focus is to dissect the regulatory programs that govern mammalian germ cell development. Specifically, I am interested in understanding how PGCs diverge from somatic lineages to establish germline competency in embryos, and how developmental cues and metabolic needs are intertwined at mitochondria to regulate spermatogonial fate decision to become sperm after birth. Empowered with in vitro differentiation platforms of pluripotent stem cells and spermatogonial stem cells, as well as in vivo genetically modified mouse models, my laboratory aims to improve our knowledge in mammalian reproduction, thereby informing the underlying genetic causes of human male infertility.