Missegregation of chromosomes during the development of germ cells is the leading cause for infertility, natural miscarriages and congenital defects (e.g., Down syndrome). These failures increase with maternal age, leading to exponential drop in fertility starting at the age of 35. In the germline a special kind of cell division, termed meiosis, reduces the chromosome number by half to create the sperm and eggs by two consecutive chromosome segregations. Over a century of studies on the subject have taught us much on this developmental process, yet our knowledge on the underlying genetics and signal transduction pathways that governs germline aging is minimal.
In our research we use human oocytes donated by patients as well as the nematode Caenorhabditis elegans as a model organism. Using C. elegans is advantageous for many reasons. One of them is that in the worm’s gonad germ cells are organized from the stem cells to the mature gametes.
Unlike mammals, aging in the worm occur within days and not years and decades. This allowed us to characterize the changes that occur in the gonad during aging, find the signals that control it, and improve the quality of mature oocytes using pharmacological tools.
You can read more about our research and current directions here.