Dynamin‐mediated lipid acquisition is essential for C hlamydia trachomatis development

Summary C hlamydia trachomatis is an obligate intracellular pathogen responsible for a high burden of human disease. Here, a loss‐of‐function screen using a set of lentivirally transduced shRNAs identified 14 human host cell factors that modulate C . trachomatis infectivity. Notably, knockdown of dynamin, a host GTPase , decreased C . trachomatis infectivity. Dynamin functions in multiple cytoplasmic locations, including vesicle formation at the plasma membrane and the trans‐ G olgi network. However, its role in C . trachomatis infection remains unclear. Here we report that dynamin is essential for homotypic fusion of C . trachomatis inclusions but not for C . trachomatis internalization into the host cell. Further, dynamin activity is necessary for lipid transport into C . trachomatis inclusions and for normal re‐differentiation from reticulate to elementary bodies. Fragmentation of the G olgi apparatus is proposed to be an important strategy used by C . trachomatis for efficient lipid acquisition and replication within the host. Here we show that a subset of C . trachomatis ‐infected cells displayed G olgi fragmentation, which was concurrent with increased mitotic accumulation. G olgi fragmentation was dispensable for dynamin‐mediated lipid acquisition into C . trachomatis inclusions, irrespective of the cell cycle phase. Thus, our study reveals a critical role of dynamin in host‐derived lipid acquisition for C . trachomatis development.