Shiao Shin-Hong, Whitten Miranda M A, Zachary Daniel, Hoffmann Jules A, Levashina Elena A
Fz2 and cdc42 mediate melanization and actin polymerization but are dispensable for Plasmodium killing in the mosquito midgut Journal Article
In: PLoS Pathog., vol. 2, no. 12, pp. e133, 2006, ISSN: 1553-7374.
Abstract | Links | BibTeX | Tags: Actins, Animals, Anopheles, Carrier Proteins, cdc42 GTP-Binding Protein, Double-Stranded, Electron, Frizzled Receptors, Gastrointestinal Tract, hoffmann, Host-Parasite Interactions, Immunity, Innate, Insect Vectors, Intestinal Mucosa, M3i, Melanins, Microarray Analysis, Microscopy, Plasmodium berghei, Polymers, Protozoan, RNA, scanning, telomerase
@article{shiao_fz2_2006,
title = {Fz2 and cdc42 mediate melanization and actin polymerization but are dispensable for Plasmodium killing in the mosquito midgut},
author = {Shin-Hong Shiao and Miranda M A Whitten and Daniel Zachary and Jules A Hoffmann and Elena A Levashina},
doi = {10.1371/journal.ppat.0020133},
issn = {1553-7374},
year = {2006},
date = {2006-12-01},
journal = {PLoS Pathog.},
volume = {2},
number = {12},
pages = {e133},
abstract = {The midgut epithelium of the mosquito malaria vector Anopheles is a hostile environment for Plasmodium, with most parasites succumbing to host defenses. This study addresses morphological and ultrastructural features associated with Plasmodium berghei ookinete invasion in Anopheles gambiae midguts to define the sites and possible mechanisms of parasite killing. We show by transmission electron microscopy and immunofluorescence that the majority of ookinetes are killed in the extracellular space. Dead or dying ookinetes are surrounded by a polymerized actin zone formed within the basal cytoplasm of adjacent host epithelial cells. In refractory strain mosquitoes, we found that formation of this zone is strongly linked to prophenoloxidase activation leading to melanization. Furthermore, we identify two factors controlling both phenomena: the transmembrane receptor frizzled-2 and the guanosine triphosphate-binding protein cell division cycle 42. However, the disruption of actin polymerization and melanization by double-stranded RNA inhibition did not affect ookinete survival. Our results separate the mechanisms of parasite killing from subsequent reactions manifested by actin polymerization and prophenoloxidase activation in the A. gambiae-P. berghei model. These latter processes are reminiscent of wound healing in other organisms, and we propose that they represent a form of wound-healing response directed towards a moribund ookinete, which is perceived as damaged tissue.},
keywords = {Actins, Animals, Anopheles, Carrier Proteins, cdc42 GTP-Binding Protein, Double-Stranded, Electron, Frizzled Receptors, Gastrointestinal Tract, hoffmann, Host-Parasite Interactions, Immunity, Innate, Insect Vectors, Intestinal Mucosa, M3i, Melanins, Microarray Analysis, Microscopy, Plasmodium berghei, Polymers, Protozoan, RNA, scanning, telomerase},
pubstate = {published},
tppubtype = {article}
}
Frolet Cécile, Thoma Martine, Blandin Stéphanie A, Hoffmann Jules A, Levashina Elena A
Boosting NF-kappaB-dependent basal immunity of Anopheles gambiae aborts development of Plasmodium berghei Journal Article
In: Immunity, vol. 25, no. 4, pp. 677–685, 2006, ISSN: 1074-7613.
Abstract | Links | BibTeX | Tags: Animals, Anopheles gambiae, blandin, Gene Expression, Gene Expression Regulation, Genes, hoffmann, Immunity, Insect, M3i, NF-kappa B, Plasmodium berghei, telomerase
@article{frolet_boosting_2006,
title = {Boosting NF-kappaB-dependent basal immunity of Anopheles gambiae aborts development of Plasmodium berghei},
author = {Cécile Frolet and Martine Thoma and Stéphanie A Blandin and Jules A Hoffmann and Elena A Levashina},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17045818},
doi = {10.1016/j.immuni.2006.08.019},
issn = {1074-7613},
year = {2006},
date = {2006-10-01},
journal = {Immunity},
volume = {25},
number = {4},
pages = {677--685},
abstract = {Anopheles gambiae, the major vector for the protozoan malaria parasite Plasmodium falciparum, mounts powerful antiparasitic responses that cause marked parasite loss during midgut invasion. Here, we showed that these antiparasitic defenses were composed of pre- and postinvasion phases and that the preinvasion phase was predominantly regulated by Rel1 and Rel2 members of the NF-kappaB transcription factors. Concurrent silencing of Rel1 and Rel2 decreased the basal expression of the major antiparasitic genes TEP1 and LRIM1 and abolished resistance of Anopheles to the rodent malaria parasite P. berghei. Conversely, depletion of a negative regulator of Rel1, Cactus, prior to infection, enhanced the basal expression of TEP1 and of other immune factors and completely prevented parasite development. Our findings uncover the crucial role of the preinvasion defense in the elimination of parasites, which is at least in part based on circulating blood molecules.},
keywords = {Animals, Anopheles gambiae, blandin, Gene Expression, Gene Expression Regulation, Genes, hoffmann, Immunity, Insect, M3i, NF-kappa B, Plasmodium berghei, telomerase},
pubstate = {published},
tppubtype = {article}
}