The Actinomyosin Motor Drives Malaria Parasite Red Blood Cell Invasion but Not Egress

ABSTRACT Apicomplexa are obligate intracellular parasites that actively invade, replicate within, and egress from host cells. The parasite actinomyosin-based molecular motor complex (often referred to as the glideosome) is considered an important mediator of parasite motility and virulence. Mature i...

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Autores principales: Abigail J. Perrin, Christine R. Collins, Matthew R. G. Russell, Lucy M. Collinson, David A. Baker, Michael J. Blackman
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Publicado: American Society for Microbiology 2018
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spelling oai:doaj.org-article:093ba9dc06054e14aab1802c0b6e09892021-11-15T16:00:14ZThe Actinomyosin Motor Drives Malaria Parasite Red Blood Cell Invasion but Not Egress10.1128/mBio.00905-182150-7511https://doaj.org/article/093ba9dc06054e14aab1802c0b6e09892018-09-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.00905-18https://doaj.org/toc/2150-7511ABSTRACT Apicomplexa are obligate intracellular parasites that actively invade, replicate within, and egress from host cells. The parasite actinomyosin-based molecular motor complex (often referred to as the glideosome) is considered an important mediator of parasite motility and virulence. Mature intracellular parasites often become motile just prior to egress from their host cells, and in some genera, this motility is important for successful egress as well as for subsequent invasion of new host cells. To determine whether actinomyosin-based motility is important in the red blood cell egress and invasion activities of the malaria parasite, we have used a conditional genetic approach to delete GAP45, a primary component of the glideosome, in asexual blood stages of Plasmodium falciparum. Our results confirm the essential nature of GAP45 for invasion but show that P. falciparum does not require a functional motor complex to undergo egress from the red blood cell. Malarial egress therefore differs fundamentally from induced egress in the related apicomplexan Toxoplasma gondii. IMPORTANCE Clinical malaria results from cycles of replication of single-celled parasites of the genus Plasmodium in red blood cells. Intracellular parasite replication is followed by a highly regulated, protease-dependent process called egress, in which rupture of the bounding membranes allows explosive release of daughter merozoites which rapidly invade fresh red cells. A parasite actinomyosin-based molecular motor (the glideosome) has been proposed to provide the mechanical force to drive invasion. Studies of the related parasite Toxoplasma gondii have shown that induced egress requires parasite motility, mediated by a functional glideosome. However, whether the glideosome has a similar essential role in egress of malaria merozoites from red blood cells is unknown. Here, we show that although a functional glideosome is required for red blood cell invasion by Plasmodium falciparum merozoites, it is not required for egress. These findings place further emphasis on the key role of the protease cascade in malarial egress.Abigail J. PerrinChristine R. CollinsMatthew R. G. RussellLucy M. CollinsonDavid A. BakerMichael J. BlackmanAmerican Society for MicrobiologyarticleGAP45Plasmodium falciparumegressglideosomeinvasionmalariaMicrobiologyQR1-502ENmBio, Vol 9, Iss 4 (2018)
institution DOAJ
collection DOAJ
language EN
topic GAP45
Plasmodium falciparum
egress
glideosome
invasion
malaria
Microbiology
QR1-502
spellingShingle GAP45
Plasmodium falciparum
egress
glideosome
invasion
malaria
Microbiology
QR1-502
Abigail J. Perrin
Christine R. Collins
Matthew R. G. Russell
Lucy M. Collinson
David A. Baker
Michael J. Blackman
The Actinomyosin Motor Drives Malaria Parasite Red Blood Cell Invasion but Not Egress
description ABSTRACT Apicomplexa are obligate intracellular parasites that actively invade, replicate within, and egress from host cells. The parasite actinomyosin-based molecular motor complex (often referred to as the glideosome) is considered an important mediator of parasite motility and virulence. Mature intracellular parasites often become motile just prior to egress from their host cells, and in some genera, this motility is important for successful egress as well as for subsequent invasion of new host cells. To determine whether actinomyosin-based motility is important in the red blood cell egress and invasion activities of the malaria parasite, we have used a conditional genetic approach to delete GAP45, a primary component of the glideosome, in asexual blood stages of Plasmodium falciparum. Our results confirm the essential nature of GAP45 for invasion but show that P. falciparum does not require a functional motor complex to undergo egress from the red blood cell. Malarial egress therefore differs fundamentally from induced egress in the related apicomplexan Toxoplasma gondii. IMPORTANCE Clinical malaria results from cycles of replication of single-celled parasites of the genus Plasmodium in red blood cells. Intracellular parasite replication is followed by a highly regulated, protease-dependent process called egress, in which rupture of the bounding membranes allows explosive release of daughter merozoites which rapidly invade fresh red cells. A parasite actinomyosin-based molecular motor (the glideosome) has been proposed to provide the mechanical force to drive invasion. Studies of the related parasite Toxoplasma gondii have shown that induced egress requires parasite motility, mediated by a functional glideosome. However, whether the glideosome has a similar essential role in egress of malaria merozoites from red blood cells is unknown. Here, we show that although a functional glideosome is required for red blood cell invasion by Plasmodium falciparum merozoites, it is not required for egress. These findings place further emphasis on the key role of the protease cascade in malarial egress.
format article
author Abigail J. Perrin
Christine R. Collins
Matthew R. G. Russell
Lucy M. Collinson
David A. Baker
Michael J. Blackman
author_facet Abigail J. Perrin
Christine R. Collins
Matthew R. G. Russell
Lucy M. Collinson
David A. Baker
Michael J. Blackman
author_sort Abigail J. Perrin
title The Actinomyosin Motor Drives Malaria Parasite Red Blood Cell Invasion but Not Egress
title_short The Actinomyosin Motor Drives Malaria Parasite Red Blood Cell Invasion but Not Egress
title_full The Actinomyosin Motor Drives Malaria Parasite Red Blood Cell Invasion but Not Egress
title_fullStr The Actinomyosin Motor Drives Malaria Parasite Red Blood Cell Invasion but Not Egress
title_full_unstemmed The Actinomyosin Motor Drives Malaria Parasite Red Blood Cell Invasion but Not Egress
title_sort actinomyosin motor drives malaria parasite red blood cell invasion but not egress
publisher American Society for Microbiology
publishDate 2018
url https://doaj.org/article/093ba9dc06054e14aab1802c0b6e0989
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