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Tina Tootle, PhD

Associate Professor of Anatomy and Cell Biology

Contact Information

1-550 Bowen Science Building
Iowa City, IA 52242

1-500 Bowen Science Building
Iowa City, IA 52242


BS, Microbiology, University of Maryland
PhD, Biology, Massachusetts Institute of Technology
Postdoctoral Fellow, Prostaglandin signaling, Carnegie Institution for Science, Department of Embryology

Education/Training Program Affiliations

Department of Cell and Developmental Graduate Program, Interdisciplinary Graduate Program in Genetics, Interdisciplinary Graduate Program in Molecular Medicine, Medical Scientist Training Program

Center, Program and Institute Affiliations

Holden Comprehensive Cancer Center

Research Summary

Prostaglandins are transiently acting lipid signals that are synthesized at their sites of action by cyclooxygenase (COX) enzymes, the targets of Aspirin and Advil, to mediate a variety of biological activities, including inflammation, sleep, reproduction, and cancer development. How do prostaglandins regulate these diverse, cellular events? To address this question we have developed Drosophila oogenesis as a new and powerful model for studying prostaglandin signaling. Using both pharmacology and genetics, we have discovered that prostaglandins mediate Drosophila follicle development, identified the Drosophila COX1 enzyme, Pxt, and revealed that genetic perturbation of prostaglandin signaling can be used to exam the function of prostaglandins. This research on prostaglandin signaling implicates it in modulating actin/membrane dynamics, cell migration, stem cell activity, and the timing of gene expression during Drosophila follicle development. The lab is currently pursuing how prostaglandin signaling regulates actin dynamics and invasive cell migrations during Drosophila follicle development. By using a multifaceted experimental approach that combines Drosophila genetics, cell biology, live imaging, and biochemistry to we can begin to work out the mechanisms by which prostaglandins regulate these processes, and provide general insight into how prostaglandins regulate the cytoskeleton and migration at a cellular level. Such mechanisms of prostaglandin action are likely to be reutilized throughout development, including mediating the changes that occur during cancer progression and metastasis. Using Drosophila we have identified a number of novel targets of prostaglandins. We are now extending our studies to use human breast cancer cell lines to determine whether these new prostaglandin targets are conserved and the roles of such targets in prostaglandin-dependent cancer development, migration, and invasion.