The N-terminus of the effector Tarp engages the host Hippo pathway.

UNLABELLED

() is an obligate, intracellular Gram-negative bacteria and the leading bacterial sexually transmitted infection in the United States. manipulates the host cell biology using various secreted bacterial effectors during its intracellular development. The early effector ranslocated ctin-ecruiting hosphoprotein (Tarp), important for entry, has a well-characterized C-terminal region which can polymerize and bundle F-actin. In contrast, not much is known about the function of the N-terminus of Tarp (N-Tarp), though present in many spp. To address this, we use as an cell biology platform to study N-Tarp-host interactions. Transgenic expression of N-Tarp in results in developmental phenotypes consistent with altered host Salvador-Warts-Hippo signaling, a conserved signaling cascade that regulates host cell proliferation and survival. We studied the N-Tarp function in larval imaginal wing discs, which are sensitive to perturbations in Hippo signaling. N-Tarp causes wing disc overgrowth and a concomitant increase in adult wing size, phenocopying overexpression of the Hippo co-activator Yorkie. N-Tarp also causes upregulation of Hippo target genes. Last, N-Tarp-induced phenotypes can be rescued by reducing the levels of Yorkie or the Hippo target genes and . Thus, we provide evidence that the N-terminal region of the effector Tarp is sufficient to alter host Hippo signaling and acts upstream of the co-activator Yorkie.

IMPORTANCE

The survival of obligate intracellular bacteria like depends on the survival of the host cell itself. It is not surprising that -infected cells are resistant to cell death, though the exact molecular mechanism is largely unknown. Here, we establish that the N-terminal region of the well-known early effector Tarp can alter Hippo signaling in vivo. Only recently implicated in infection, the Hippo pathway is known to promote cell survival. Our findings illuminate one possible mechanism for to promote host cell survival during infection. We further demonstrate the utility of as a tool in the study of effector function.