Actin-Based Motility of Intracellular Microbial Pathogens

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Published inMicrobiology and Molecular Biology Reviews Vol. 65; no. 4; pp. 595 - 626
Main Author Goldberg, Marcia B.
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.12.2001
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Abstract Article Usage Stats Services MMBR Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue MMBR About MMBR Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MMBR RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 1092-2172 Online ISSN: 1098-5557 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MMBR .asm.org, visit: MMBR       
AbstractList A diverse group of intracellular microorganisms, including Listeria monocytogenes, Shigella spp., Rickettsia spp., and vaccinia virus, utilize actin-based motility to move within and spread between mammalian host cells. These organisms have in common a pathogenic life cycle that involves a stage within the cytoplasm of mammalian host cells. Within the cytoplasm of host cells, these organisms activate components of the cellular actin assembly machinery to induce the formation of actin tails on the microbial surface. The assembly of these actin tails provides force that propels the organisms through the cell cytoplasm to the cell periphery or into adjacent cells. Each of these organisms utilizes preexisting mammalian pathways of actin rearrangement to induce its own actin-based motility. Particularly remarkable is that while all of these microbes use the same or overlapping pathways, each intercepts the pathway at a different step. In addition, the microbial molecules involved are each distinctly different from the others. Taken together, these observations suggest that each of these microbes separately and convergently evolved a mechanism to utilize the cellular actin assembly machinery. The current understanding of the molecular mechanisms of microbial actin-based motility is the subject of this review.
Article Usage Stats Services MMBR Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue MMBR About MMBR Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MMBR RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 1092-2172 Online ISSN: 1098-5557 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MMBR .asm.org, visit: MMBR       
A diverse group of intracellular microorganisms, including Listeria monocytogenes, Shigella spp., Rickettsia spp., and vaccinia virus, utilize actin-based motility to move within and spread between mammalian host cells. These organisms have in common a pathogenic life cycle that involves a stage within the cytoplasm of mammalian host cells. Within the cytoplasm of host cells, these organisms activate components of the cellular actin assembly machinery to induce the formation of actin tails on the microbial surface. The assembly of these actin tails provides force that propels the organisms through the cell cytoplasm to the cell periphery or into adjacent cells. Each of these organisms utilizes preexisting mammalian pathways of actin rearrangement to induce its own actin-based motility. Particularly remarkable is that while all of these microbes use the same or overlapping pathways, each intercepts the pathway at a different step. In addition, the microbial molecules involved are each distinctly different from the others. Taken together, these observations suggest that each of these microbes separately and convergently evolved a mechanism to utilize the cellular actin assembly machinery. The current understanding of the molecular mechanisms of microbial actin-based motility is the subject of this review.A diverse group of intracellular microorganisms, including Listeria monocytogenes, Shigella spp., Rickettsia spp., and vaccinia virus, utilize actin-based motility to move within and spread between mammalian host cells. These organisms have in common a pathogenic life cycle that involves a stage within the cytoplasm of mammalian host cells. Within the cytoplasm of host cells, these organisms activate components of the cellular actin assembly machinery to induce the formation of actin tails on the microbial surface. The assembly of these actin tails provides force that propels the organisms through the cell cytoplasm to the cell periphery or into adjacent cells. Each of these organisms utilizes preexisting mammalian pathways of actin rearrangement to induce its own actin-based motility. Particularly remarkable is that while all of these microbes use the same or overlapping pathways, each intercepts the pathway at a different step. In addition, the microbial molecules involved are each distinctly different from the others. Taken together, these observations suggest that each of these microbes separately and convergently evolved a mechanism to utilize the cellular actin assembly machinery. The current understanding of the molecular mechanisms of microbial actin-based motility is the subject of this review.
A diverse group of intracellular microorganisms, including Listeria monocytogenes, Shigella spp., Rickettsia spp., and vaccinia virus, utilize actin-based motility to move within and spread between mammalian host cells. These organisms have in common a pathogenic life cycle that involves a stage within the cytoplasm of mammalian host cells.
Author Marcia B. Goldberg
AuthorAffiliation Infectious Disease Division, Massachusetts General Hospital, Boston, Massachusetts 02114
AuthorAffiliation_xml – name: Infectious Disease Division, Massachusetts General Hospital, Boston, Massachusetts 02114
Author_xml – sequence: 1
  givenname: Marcia B.
  surname: Goldberg
  fullname: Goldberg, Marcia B.
  organization: <!--label omitted: 1-->Infectious Disease Division, Massachusetts General Hospital, Boston, Massachusetts 02114
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14162498$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/11729265$$D View this record in MEDLINE/PubMed
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Issue 4
Keywords Motility
Life cycle
Actin
Pathogenic
Bacteria
Rickettsia
Cell
Vaccinia
Enterobacteriaceae
Chordopoxvirinae
Life history
Orthopoxvirus
Listeria monocytogenes
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Rickettsiales
Virus
Pathogenicity
Vaccinia virus
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Poxviridae
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Rickettsiaceae
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Snippet Article Usage Stats Services MMBR Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
A diverse group of intracellular microorganisms, including Listeria monocytogenes, Shigella spp., Rickettsia spp., and vaccinia virus, utilize actin-based...
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StartPage 595
SubjectTerms actin
Actins - physiology
Animal, plant and microbial ecology
Bacteriology
Biological and medical sciences
Cell Movement - physiology
Cells
Cellular biology
Fundamental and applied biological sciences. Psychology
Humans
Life cycles
Listeria - pathogenicity
Listeria - physiology
Listeria monocytogenes
Mammals
Microbial ecology
Microbiology
Microorganisms
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Pathogens
Rickettsia
Rickettsia - pathogenicity
Rickettsia - physiology
Shigella
Shigella - pathogenicity
Shigella - physiology
Transportation
Vaccinia virus
Vaccinia virus - pathogenicity
Vaccinia virus - physiology
Various environments (extraatmospheric space, air, water)
Viruses
Title Actin-Based Motility of Intracellular Microbial Pathogens
URI http://mmbr.asm.org/content/65/4/595.abstract
https://www.ncbi.nlm.nih.gov/pubmed/11729265
https://www.proquest.com/docview/231166181
https://www.proquest.com/docview/18222591
https://www.proquest.com/docview/72317554
https://pubmed.ncbi.nlm.nih.gov/PMC99042
Volume 65
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