Baltimore, MD—New work from Carnegie’s Ethan Greenblatt and Allan Spradling reveals that the genetic factors underlying fragile X syndrome, and potentially other autism-related disorders, stem from defects in the cell’s ability to create unusually large protein structures. Their findings are published in Science.
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My laboratory studies the biology of reproduction. Eggs are remarkable cells, that by unknown means reset the normally irreversible processes of differentiation and aging that govern all somatic cells. We use Drosophila as our primary research system, because these processes are likely to be conserved in all metazoan organisms and Drosophila currently provides the experimentally most favorable multicellular system for molecular genetic studies. We focus on several aspects of oogenesis that promise to provide insight into nuclear and cytoplasmic rejuvenation. By studying ovarian stem cells, we are learning how cells maintain an undifferentiated state and how cell production is regulated by microenvironments known as niches. We have found that epithelial stem cells responsible for follicle cell production compete. Replacement of damaged stem cells may be a major mechanism that limits somatic mutation, but we have also found that mutations exist that confer the ability to replace wild type cells. Such mutations may be precursors to cellular aging and cancer. We also believe that an elaborate system of organelle sorting during the time germ cells are interconnected prior to meiosis contributes to the removal of damaged mitochondrial DNA molecules, and possibly also acts on damaged proteins. Finally, in order to understand better how these complex processes are controlled, we are re-investigating the role of steroid and prostaglandin hormones in controlling the process of oogenesis, from stem cell to laid egg.