Elizabeth (Lisa) Rucks, PhD

ELIZABETH (Lisa) Rucks, PhD
Associate Professor

BS, College of Charleston
PhD, West Virginia University
Postdoctoral training, Rocky Mountain Laboratory, NIAID


In our lab, we study the fascinating and highly successful obligate intracellular pathogen, Chlamydia trachomatis, the organism which causes the most common bacterial sexually transmitted infection and is also the leading cause of preventable blindness in developing countries. Despite having a genome 1/4 of the size of a pathogenic E. coli, Chlamydia adeptly infect the host while limiting the host response to infection.

Chlamydiae are also unique in that they have a biphasic developmental cycle. They infect cells only while in their elementary body (EB) form. From the time that the organisms enter host cells until the time that they exit, they grow and develop within a membrane bound vacuole termed the inclusion. Within the first hour of infection, the EB differentiates into the reticulate body (RB). The RB is not infectious, but is metabolically active and divides by a newly described polarized budding method. To maintain its autonomy, the chlamydial inclusion interacts with very specific host cell pathways, which ultimately influences the lipid and protein content of the inclusion. Paramount to chlamydial survival within the host is the organism’s ability to obtain and utilize host cell-derived lipids. These lipids contribute to the membrane of the chlamydial inclusion, as well as, the chlamydial cell membranes. It is well established that Chlamydia will mimic the lipid composition of their host cells, but the organisms will not incorporate all available host-derived lipids into their cell membranes. We are interested in understanding how and why this phenomenon happens and, ultimately, understand how these activities contribute to their success as pathogens. 


Olson MG, Ouellette SP, Rucks EA. A meta-analysis of affinity purification-mass spectrometry experimental systems used to identify eukaryotic and chlamydial proteins at the chlamydial inclusion membrane. J. Proteomics. 2020 212, 103595. PMID: 31760040.

Olson MG, Widner RE, Jorgenson LM, Lawrence A, Lagundzin D, Woods NT, Ouellette SP#, Rucks EA#. Proximity labeling to map host-pathogen interactions at the membrane of a bacteria containing vacuole in Chlamydia trachomatis infected human cells. Infect. Immun., 2019 87(11): e000537-19. PMID: 31405957.

Rucks EA, Olson MG, Jorgenson LM, Srinivasan RR, and Ouellette SP. Development of a proximity labeling system to map the Chlamydia trachomatis inclusion membrane. Front. Cell. Infect. Microbiol. 7: 40, 2017. doi:10.3389/fcimb.2017.00040 PMID: 28261569

Moore ER and SP Ouellette. Reconceptualizing the chlamydial inclusion as a pathogen specified parasitic organelle: an expanded role for Inc proteins. Front. Cell. Infect. Microbiol. 4: 157, 2014. PMID: 25401095

Lucas AL, SP Ouellette, EJ Kabeiseman, K Cichos^, and EA Rucks. The trans-Golgi SNARE syntaxin 10 is required for optimal development of Chlamydia trachomatis. Front. Cell. Infect. Microbiol. 5:68,  2015. PMID: 26442221

Kabeiseman EJ, KH Cichos, and ER Moore. The eukaryotic signal sequence, YGRL, targets the chlamydial inclusion. Front. Cell. Infect. Microbiol. 4:129, 2014. PMID: 25309881

Kabeiseman EJ, K Cichos, T Hackstadt, A Lucas, and ER Moore. Vesicle-associated membrane protein 4 and syntaxin 6 interactions at the chlamydial inclusion. Infect. Immun. 81: 3326-3337, 2013. PMID: 23798538

Moore ER, DJ Mead, CA Dooley, J Sager, T Hackstadt. The trans-Golgi SNARE syntaxin 6 is recruited to the chlamydial inclusion membrane. Microbiology, 157: 830-838, 2011. PMID: 21109560

Moore ER, ER Fischer, DJ Mead, T Hackstadt. The chlamydial inclusion preferentially intercepts basolaterally directed sphingomyelin-containing exocytic vacuoles. Traffic, 9: 2130-2140, 2008. PMID: 18778406