@article{SunkavalliAguilarSilvaetal.2017,
  author    = {Sunkavalli, Ushasree and Aguilar, Carmen and Silva, Ricardo Jorge and Sharan, Malvika and Cruz, Ana Rita and Tawk, Caroline and Maudet, Claire and Mano, Miguel and Eulalio, Ana},
  title     = {Analysis of host microRNA function uncovers a role for miR-29b-2-5p in Shigella capture by filopodia},
  series = {PLoS Pathogens},
  volume    = {13},
  journal   = {PLoS Pathogens},
  number    = {4},
  doi       = {10.1371/journal.ppat.1006327},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-158204},
  pages     = {e1006327},
  year      = {2017},
  abstract  = {MicroRNAs play an important role in the interplay between bacterial pathogens and host cells, participating as host defense mechanisms, as well as exploited by bacteria to subvert host cellular functions. Here, we show that microRNAs modulate infection by Shigella flexneri, a major causative agent of bacillary dysentery in humans. Specifically, we characterize the dual regulatory role of miR-29b-2-5p during infection, showing that this microRNA strongly favors Shigella infection by promoting both bacterial binding to host cells and intracellular replication. Using a combination of transcriptome analysis and targeted high-content RNAi screening, we identify UNC5C as a direct target of miR-29b-2-5p and show its pivotal role in the modulation of Shigella binding to host cells. MiR-29b-2-5p, through repression of UNC5C, strongly enhances filopodia formation thus increasing Shigella capture and promoting bacterial invasion. The increase of filopodia formation mediated by miR-29b-2-5p is dependent on RhoF and Cdc42 Rho-GTPases. Interestingly, the levels of miR-29b-2-5p, but not of other mature microRNAs from the same precursor, are decreased upon Shigella replication at late times post-infection, through degradation of the mature microRNA by the exonuclease PNPT1. While the relatively high basal levels of miR-29b-2-5p at the start of infection ensure efficient Shigella capture by host cell filopodia, dampening of miR-29b-2-5p levels later during infection may constitute a bacterial strategy to favor a balanced intracellular replication to avoid premature cell death and favor dissemination to neighboring cells, or alternatively, part of the host response to counteract Shigella infection. Overall, these findings reveal a previously unappreciated role of microRNAs, and in particular miR-29b-2-5p, in the interaction of Shigella with host cells.},
  language  = {en}
}
@article{EulalioFroehlichManoetal.2011,
  author    = {Eulalio, Ana and Fr{\"o}hlich, Kathrin S. and Mano, Miguel and Giacca, Mauro and Vogel, J{\"o}rg},
  title     = {A Candidate Approach Implicates the Secreted Salmonella Effector Protein SpvB in P-Body Disassembly},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-68928},
  year      = {2011},
  abstract  = {P-bodies are dynamic aggregates of RNA and proteins involved in several post-transcriptional regulation processes. Pbodies have been shown to play important roles in regulating viral infection, whereas their interplay with bacterial pathogens, specifically intracellular bacteria that extensively manipulate host cell pathways, remains unknown. Here, we report that Salmonella infection induces P-body disassembly in a cell type-specific manner, and independently of previously characterized pathways such as inhibition of host cell RNA synthesis or microRNA-mediated gene silencing. We show that the Salmonella-induced P-body disassembly depends on the activation of the SPI-2 encoded type 3 secretion system, and that the secreted effector protein SpvB plays a major role in this process. P-body disruption is also induced by the related pathogen, Shigella flexneri, arguing that this might be a new mechanism by which intracellular bacterial pathogens subvert host cell function.},
  subject      = {Salmonella},
  language  = {en}
}