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Citation
Lee, K.Z., Lestradet, M., Socha, C., Schirmeier, S., Schmitz, A., Spenlé, C., Lefebvre, O., Keime, C., Yamba, W.M., Bou Aoun, R., Liegeois, S., Schwab, Y., Simon-Assmann, P., Dalle, F., Ferrandon, D. (2016). Enterocyte Purge and Rapid Recovery Is a Resilience Reaction of the Gut Epithelium to Pore-Forming Toxin Attack.  Cell Host Microbe 20(6): 716--730.
FlyBase ID
FBrf0234229
Publication Type
Research paper
Abstract
Besides digesting nutrients, the gut protects the host against invasion by pathogens. Enterocytes may be subjected to damage by both microbial and host defensive responses, causing their death. Here, we report a rapid epithelial response that alleviates infection stress and protects the enterocytes from the action of microbial virulence factors. Intestinal epithelia exposed to hemolysin, a pore-forming toxin secreted by Serratia marcescens, undergo an evolutionarily conserved process of thinning followed by the recovery of their initial thickness within a few hours. In response to hemolysin attack, Drosophila melanogaster enterocytes extrude most of their apical cytoplasm, including damaged organelles such as mitochondria, yet do not lyse. We identify two secreted peptides, the expression of which requires CyclinJ, that mediate the recovery phase in which enterocytes regain their original shape and volume. Epithelial thinning and recovery constitute a fast and efficient response to intestinal infections, with pore-forming toxins acting as alarm signals.
Graphical Abstract
Obtained with permission from Cell Press.
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PubMed Central ID
Related Publication(s)
Note

Pore-Forming Toxins Trigger the Purge.
Bonfini and Buchon, 2016, Cell Host Microbe 20(6): 693--694 [FBrf0234308]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Cell Host Microbe
    Title
    Cell Host & Microbe
    Publication Year
    2007--
    ISBN/ISSN
    1931-3128 1934-6069
    Data From Reference
    Aberrations (1)
    Alleles (16)
    Chemicals (1)
    Genes (16)
    Human Disease Models (1)
    Natural transposons (1)
    Insertions (2)
    Experimental Tools (2)
    Transgenic Constructs (13)
    Transcripts (1)