<i>Chlamydia trachomatis</i> TmeA promotes pedestal-like structure formation through N-WASP and TOCA-1 interactions

<i>Chlamydia trachomatis</i> (<i>C.t.</i>) is an obligate intracellular bacterial pathogen that poses a significant threat to human health, being associated with various diseases, including chlamydia-the most prevalent bacterial sexually transmitted infection-and trachoma. Although often asymptomatic, chlamydia infections can lead to severe complications, such as infertility, ectopic pregnancy, and an increased risk of cervical and ovarian cancers. As an intracellular pathogen, host cell invasion is critical for <i>C.t.</i> survival and pathogenesis. In this study, we provide new insights into the interactions between the <i>C.t.</i> invasion effector protein TmeA and the host proteins N-WASP and TOCA-1, revealing that both host proteins are involved in pedestal-like structure formation during early stages of <i>C.t.</i> infection. These findings deepen our understanding of the mechanisms underlying TmeA-mediated host cell invasion and highlight a key pathway contributing to <i>C.t.</i>-mediated pathogenesis.