Document Detail


Non-lytic, actin-based exit of intracellular parasites from C. elegans intestinal cells.
MedLine Citation:
PMID:  21949650     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The intestine is a common site for invasion by intracellular pathogens, but little is known about how pathogens restructure and exit intestinal cells in vivo. The natural microsporidian parasite N. parisii invades intestinal cells of the nematode C. elegans, progresses through its life cycle, and then exits cells in a transmissible spore form. Here we show that N. parisii causes rearrangements of host actin inside intestinal cells as part of a novel parasite exit strategy. First, we show that N. parisii infection causes ectopic localization of the normally apical-restricted actin to the basolateral side of intestinal cells, where it often forms network-like structures. Soon after this actin relocalization, we find that gaps appear in the terminal web, a conserved cytoskeletal structure that could present a barrier to exit. Reducing actin expression creates terminal web gaps in the absence of infection, suggesting that infection-induced actin relocalization triggers gap formation. We show that terminal web gaps form at a distinct stage of infection, precisely timed to precede spore exit, and that all contagious animals exhibit gaps. Interestingly, we find that while perturbations in actin can create these gaps, actin is not required for infection progression or spore formation, but actin is required for spore exit. Finally, we show that despite large numbers of spores exiting intestinal cells, this exit does not cause cell lysis. These results provide insight into parasite manipulation of the host cytoskeleton and non-lytic escape from intestinal cells in vivo.
Authors:
Kathleen A Estes; Suzannah C Szumowski; Emily R Troemel
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-09-15
Journal Detail:
Title:  PLoS pathogens     Volume:  7     ISSN:  1553-7374     ISO Abbreviation:  PLoS Pathog.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-28     Completed Date:  2012-02-29     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  101238921     Medline TA:  PLoS Pathog     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e1002227     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Actin Cytoskeleton / metabolism*,  microbiology
Animals
Caenorhabditis elegans / cytology,  microbiology*
Host-Pathogen Interactions
Intestines / cytology,  parasitology
Microfilament Proteins / metabolism
Microsporidia / metabolism,  pathogenicity*
RNA Interference
RNA, Small Interfering
Spores, Fungal / metabolism*
Grant Support
ID/Acronym/Agency:
5T32AI060536/AI/NIAID NIH HHS; AI087528/AI/NIAID NIH HHS; P30 AI036214/AI/NIAID NIH HHS; R01 AI087528/AI/NIAID NIH HHS; R01 AI087528-03/AI/NIAID NIH HHS; T32GM008666/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Microfilament Proteins; 0/RNA, Small Interfering
Comments/Corrections

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