Dynamin-dependent entry of Chlamydia trachomatis is sequentially regulated by the effectors TarP and TmeA

Matthew D. Romero and Rey A. Carabeo ()
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Matthew D. Romero: University of Nebraska Medical Center
Rey A. Carabeo: University of Nebraska Medical Center

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract Chlamydia invasion of epithelial cells is a pathogen-driven process involving two functionally distinct effectors – TarP and TmeA. They collaborate to promote robust actin dynamics at sites of entry. Here, we extend studies on the molecular mechanism of invasion by implicating the host GTPase dynamin 2 (Dyn2) in the completion of pathogen uptake. Importantly, Dyn2 function is modulated by TarP and TmeA at the levels of recruitment and activation through oligomerization, respectively. TarP-dependent recruitment requires phosphatidylinositol 3-kinase and the small GTPase Rac1, while TmeA has a post-recruitment role related to Dyn2 oligomerization. This is based on the rescue of invasion duration and efficiency in the absence of TmeA by the Dyn2 oligomer-stabilizing small molecule activator Ryngo 1-23. Notably, Dyn2 also regulated turnover of TarP- and TmeA-associated actin networks, with disrupted Dyn2 function resulting in aberrant turnover dynamics, thus establishing the interdependent functional relationship between Dyn2 and the effectors TarP and TmeA.

Date: 2024
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DOI: 10.1038/s41467-024-49350-6

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