Intranuclear niche: actin-tail mediated nuclear entry by intracellular pathogens

Authors

Cheung, H. C., Reist Iscar, P., Plum, M. T. W., Basler, M.

Abstract

Intracellular pathogens localize to various niches in the host cells to avoid immune detection. However, very little is known about bacteria that enter the host nuclei. Here we report that Burkholderia thailandensis, a facultative intracellular pathogen, can enter eukaryotic nuclei and replicate. Nuclear invasion events were rare, occurring 1 in 500-1,000 infected cells, and inhibition of cell division further reduced the frequency of these events. Moreover, we show that nuclear entry requires actin tail motility, although it is independent of other virulence factors such as the Type III Secretion System, Type VI Secretion System-5, and flagella motility. Inactivation of actin tail motility by deleting bimA or inhibition of actin polymerisation by cytochalasin D abolished nuclear entry. Surprisingly, we observed that accumulation of B. thailandensis in the nucleus activated assembly of the Type VI Secretion Systems-5. We further show that Shigella flexneri also enters nucleus in an actin polymerization dependent mechanism. Together, we show that actin tail forming intracellular pathogens occasionally localize to the nucleus, and while this largely requires host cell division, it may provide pathogens with a protective niche in certain mitotically active cells, such as skin, gut or epithelial cells.

Preprint server: bioRxiv
The authors list and abstract were imported from bioRxiv on 25 Aug 2026.

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