Apical membrane antigen 1 mediates apicomplexan parasite attachment but is dispensable for host cell invasion

Daniel Y. Bargieri, Nicole Andenmatten, Vanessa Lagal, Sabine Thiberge, Jamie A. Whitelaw, Isabelle Tardieux (), Markus Meissner () and Robert Ménard ()
Additional contact information
Daniel Y. Bargieri: Institut Pasteur, Malaria Biology and Genetics Unit
Nicole Andenmatten: Institute of Infection, Immunity and Inflammation, Wellcome Centre for Molecular Parasitology, Glasgow Biomedical Research Centre, University of Glasgow
Vanessa Lagal: Laboratory Barriers and Pathogens, Institut Cochin, INSERM U-1016, CNRS UMR-8104, University of Paris Descartes
Sabine Thiberge: Institut Pasteur, Malaria Biology and Genetics Unit
Jamie A. Whitelaw: Institute of Infection, Immunity and Inflammation, Wellcome Centre for Molecular Parasitology, Glasgow Biomedical Research Centre, University of Glasgow
Isabelle Tardieux: Laboratory Barriers and Pathogens, Institut Cochin, INSERM U-1016, CNRS UMR-8104, University of Paris Descartes
Markus Meissner: Institute of Infection, Immunity and Inflammation, Wellcome Centre for Molecular Parasitology, Glasgow Biomedical Research Centre, University of Glasgow
Robert Ménard: Institut Pasteur, Malaria Biology and Genetics Unit

Nature Communications, 2013, vol. 4, issue 1, 1-13

Abstract: Abstract Apicomplexan parasites invade host cells by forming a ring-like junction with the cell surface and actively sliding through the junction inside an intracellular vacuole. Apical membrane antigen 1 is conserved in apicomplexans and a long-standing malaria vaccine candidate. It is considered to have multiple important roles during host cell penetration, primarily in structuring the junction by interacting with the rhoptry neck 2 protein and transducing the force generated by the parasite motor during internalization. Here, we generate Plasmodium sporozoites and merozoites and Toxoplasma tachyzoites lacking apical membrane antigen 1, and find that the latter two are impaired in host cell attachment but the three display normal host cell penetration through the junction. Therefore, apical membrane antigen 1, rather than an essential invasin, is a dispensable adhesin of apicomplexan zoites. These genetic data have implications on the use of apical membrane antigen 1 or the apical membrane antigen 1–rhoptry neck 2 interaction as targets of intervention strategies against malaria or other diseases caused by apicomplexans.

Date: 2013
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms3552 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3552

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms3552

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().