Chlamydia trachomatis is a leading cause of sexually transmitted infections worldwide. As an obligate intracellular pathogen, it has been selected to establish a niche within the host cell in a membrane-derived vacuole called the chlamydial inclusion. Chlamydial proteins recruit host proteins to the chlamydial inclusion that are critical for infection development. Two of these host-derived chlamydial inclusion proteins include FLI1 and LRRF1. Dr. Natalie Sturd and her PI and mentor, Dr. Lisa Rucks, identified that the FLI1 and LRRF1 localization was dependent upon the chlamydial effector ct226 and that FLI1 localization was independent of LRRF1 localization. However, FLI1 co-immunoprecipitated with Ct226 but only in the presence of LRRF1 suggesting that these proteins have both independent and overlapping mechanisms for localization. Article can be read here. Dr. Sturd is current an M3 trainee in the MD/PhD scholars’ program and defended her dissertation in January of 2024.
Dr. Sturd publishes a first author manuscript in mSphere
Natalie Sturd, MD/PhD trainee