Our main interest is to understand molecular and cellular mechanisms underlying bacterial virulence. We study processes by which intracellular bacterial pathogens alter the normal functioning of eukaryotic host cells.
We focus in a virulence mechanism consisting in the injection of bacterial effector proteins into host cells through specialized secretion systems. These effectors have been shown to act on a vast array of eukaryotic cell functions. Our main research focus has been to study the function of effectors from bacterial pathogens that cause relevant infections in humans (Chlamydia and Legionella) and which possess type III or type IV secretion systems essential for their virulence.
How do bacterial proteins act on host eukaryotic cell processes to mediate virulence?
Chlamydia trachomatis delivers more than 70 effectors into host cells. We found one effector protein (CteG) that localizes at the Golgi and plasma membrane of infected host cells at different times of infection. Furthermore, many C. trachomatis effectors (Incs) are inserted into the vacuolar membrane that encloses intracellular chlamydiae.
We have been focused on how CteG is directed to distinct subcellular locations and the functions it might have there, and on Incs that might mediate lipid acquisition by chlamydiae and interfere with the microtubule cytoskeleton to position the chlamydial vacuole and facilitate interactions with the host vesicular transport pathways.
- “Identification and characterization of Chlamydia trachomatis virulence proteins”, FCT-MCTES, Total and Unit funding: €239,075, Jaime Mota (PI)
- “A multidisciplinary approach to study Chlamydia trachomatis inclusion membrane (Inc) proteins”, FCT-MCTES, Total and Unit funding: €199,236, Jaime Mota (PI)
- “Identification of new virulence mechanisms of a Legionella pneumophila strain recently isolated from a major outbreak in Portugal”, ESCMID, Total and Unit funding: €20,000, Irina Franco (PI)
Bugalhao, JN; Mota, LJ. 2019. The multiple functions of the numerous Chlamydia trachomatis secreted proteins: the tip of the iceberg. MICROBIAL CELL, 6, DOI: 10.15698/mic2019.09.691
Pais, SV; Key, CE; Borges, V; Pereira, IS; Gomes, JP; Fisher, DJ; Mota, LJ. 2019. CteG is a Chlamydia trachomatis effector protein that associates with the Golgi complex of infected host cells. Scientific Reports, 9, DOI: 10.1038/s41598-019-42647-3
Yu, XJ; Grabe, GJ; Liu, M; Mota, LJ; Holden, DW. 2018. SsaV Interacts with SsaL to Control the Translocon-to-Effector Switch in the Salmonella SPI-2 Type Three Secretion System. mBio, 9, DOI: 10.1128/mBio.01149-18
Almeida, F; Luis, MP; Pereira, IS; Pais, SV; Mota, LJ. 2018. The Human Centrosomal Protein CCDC146 Binds Chlamydia trachomatis Inclusion Membrane Protein CT288 and Is Recruited to the Periphery of the Chlamydia-Containing Vacuole. Frontiers in Cellular and Infection Microbiology, 8, DOI: 10.3389/fcimb.2018.00254
da Cunha, M; Pais, SV; Bugalhao, JN; Mota, LJ. 2017. The Chlamydia trachomatis type III secretion substrates CT142, CT143, and CT144 are secreted into the lumen of the inclusion. PLoS One, 12, DOI: 10.1371/journal.pone.0178856