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Actin depolymerizing factor controls actin turnover and gliding motility in Toxoplasma gondii
Apicomplexan parasites rely on actin-based gliding motility to move across the substratum, cross biological barriers, and invade their host cells. Gliding motility depends on polymerization of parasite actin filaments, yet ∼98% of actin is nonfilamentous in resting parasites. Previous studies sugges...
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Formato: | Texto |
Lenguaje: | English |
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The American Society for Cell Biology
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078074/ https://www.ncbi.nlm.nih.gov/pubmed/21346192 http://dx.doi.org/10.1091/mbc.E10-12-0939 |
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author | Mehta, Simren Sibley, L. David |
author_facet | Mehta, Simren Sibley, L. David |
author_sort | Mehta, Simren |
collection | PubMed |
description | Apicomplexan parasites rely on actin-based gliding motility to move across the substratum, cross biological barriers, and invade their host cells. Gliding motility depends on polymerization of parasite actin filaments, yet ∼98% of actin is nonfilamentous in resting parasites. Previous studies suggest that the lack of actin filaments in the parasite is due to inherent instability, leaving uncertain the role of actin-binding proteins in controlling dynamics. We have previously shown that the single allele of Toxoplasma gondii actin depolymerizing factor (TgADF) has strong actin monomer–sequestering and weak filament-severing activities in vitro. Here we used a conditional knockout strategy to investigate the role of TgADF in vivo. Suppression of TgADF led to accumulation of actin-rich filaments that were detected by immunofluorescence and electron microscopy. Parasites deficient in TgADF showed reduced speed of motility, increased aberrant patterns of motion, and inhibition of sustained helical gliding. Lack of TgADF also led to severe defects in entry and egress from host cells, thus blocking infection in vitro. These studies establish that the absence of stable actin structures in the parasite are not simply the result of intrinsic instability, but that TgADF is required for the rapid turnover of parasite actin filaments, gliding motility, and cell invasion. |
format | Text |
id | pubmed-3078074 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-30780742011-06-30 Actin depolymerizing factor controls actin turnover and gliding motility in Toxoplasma gondii Mehta, Simren Sibley, L. David Mol Biol Cell Articles Apicomplexan parasites rely on actin-based gliding motility to move across the substratum, cross biological barriers, and invade their host cells. Gliding motility depends on polymerization of parasite actin filaments, yet ∼98% of actin is nonfilamentous in resting parasites. Previous studies suggest that the lack of actin filaments in the parasite is due to inherent instability, leaving uncertain the role of actin-binding proteins in controlling dynamics. We have previously shown that the single allele of Toxoplasma gondii actin depolymerizing factor (TgADF) has strong actin monomer–sequestering and weak filament-severing activities in vitro. Here we used a conditional knockout strategy to investigate the role of TgADF in vivo. Suppression of TgADF led to accumulation of actin-rich filaments that were detected by immunofluorescence and electron microscopy. Parasites deficient in TgADF showed reduced speed of motility, increased aberrant patterns of motion, and inhibition of sustained helical gliding. Lack of TgADF also led to severe defects in entry and egress from host cells, thus blocking infection in vitro. These studies establish that the absence of stable actin structures in the parasite are not simply the result of intrinsic instability, but that TgADF is required for the rapid turnover of parasite actin filaments, gliding motility, and cell invasion. The American Society for Cell Biology 2011-04-15 /pmc/articles/PMC3078074/ /pubmed/21346192 http://dx.doi.org/10.1091/mbc.E10-12-0939 Text en © 2011 Sibley et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,“ “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology. |
spellingShingle | Articles Mehta, Simren Sibley, L. David Actin depolymerizing factor controls actin turnover and gliding motility in Toxoplasma gondii |
title | Actin depolymerizing factor controls actin turnover and gliding motility in Toxoplasma gondii |
title_full | Actin depolymerizing factor controls actin turnover and gliding motility in Toxoplasma gondii |
title_fullStr | Actin depolymerizing factor controls actin turnover and gliding motility in Toxoplasma gondii |
title_full_unstemmed | Actin depolymerizing factor controls actin turnover and gliding motility in Toxoplasma gondii |
title_short | Actin depolymerizing factor controls actin turnover and gliding motility in Toxoplasma gondii |
title_sort | actin depolymerizing factor controls actin turnover and gliding motility in toxoplasma gondii |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078074/ https://www.ncbi.nlm.nih.gov/pubmed/21346192 http://dx.doi.org/10.1091/mbc.E10-12-0939 |
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