ArticleNature communications2026
A pore-forming toxin initiates ABI1 complex switching to promote bacterial cell-to-cell spread.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Listeria monocytogenes (Lm), a prototypical intracellular bacterial pathogen, expresses ActA to initiate ARP2/3-mediated actin-based motility in the cytosol of host cells. Motile bacteria generate Lm-containing protrusions at the cell surface, facilitating direct cell-to-cell spread and dissemination within the host. Protrusion formation is an active, spatially regulated process, yet how Lm coordinates bacterial and host factors to orchestrate this process remains unclear. Here, we identify Abelson-interactor 1 (ABI1) as a host factor required for efficient Lm protrusion formation and cell-to-cell spread. Conditional knockout of Abi1 in mice significantly reduces susceptibility to Lm infection, while deletion of actA abrogates the protective effect of Abi1 knockout. During Lm infection, ABI1 is uncoupled from spectrin at the cell cortex and binds to EPS8 within protrusions. This ABI1 "complex switching" is initiated by the pore-forming toxin LLO, which perforates the host plasma membrane and triggers Ca
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