A monoclonal antibody that interferes with the post‐aggregation adhesion of <i>Dictyostelium discoideum</i> cells

Keller, Thomas; Eitle, Eveline; Balding, Kirsten; Corrick, C M; Parish, Roger W.

doi:10.1016/0014-5793(94)80397-8

Cited by 4 publications

(1 citation statement)

References 47 publications

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“…N-linked glycosylation is known to play a pivotal role in in the folding, quality control, stability, and function of surface and secreted proteins (21,22). It also can be a determinant of signal transduction and host-pathogen interactions (23) and has been implicated in density sensing and adhesion during the development and swarming behavior of Dictyostelium (24)(25)(26).…”

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A Glycosylation Mutant of Trypanosoma brucei Links Social Motility Defects In Vitro to Impaired Colonization of Tsetse Flies In Vivo

Imhof

Bütikofer

et al. 2015

Eukaryot Cell

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Transmission of African trypanosomes by tsetse flies requires that the parasites migrate out of the midgut lumen and colonize the ectoperitrophic space. Early procyclic culture forms correspond to trypanosomes in the lumen; on agarose plates they exhibit social motility, migrating en masse as radial projections from an inoculation site. We show that an Rft1 ؊/؊ mutant needs to reach a greater threshold number before migration begins, and that it forms fewer projections than its wild-type parent. The mutant is also up to 4 times less efficient at establishing midgut infections. Ectopic expression of Rft1 rescues social motility defects and restores the ability to colonize the fly. These results are consistent with social motility reflecting movement to the ectoperitrophic space, implicate N-glycans in the signaling cascades for migration in vivo and in vitro, and provide the first evidence that parasite-parasite interactions determine the success of transmission by the insect host.T setse flies (Glossina spp.) are the definitive hosts of the unicellular parasite Trypanosoma brucei, while a variety of mammals can serve as intermediate hosts. Different subspecies of T. brucei cause sleeping sickness in humans and Nagana in domestic animals. The passage of T. brucei through the tsetse fly was memorably described as a "journey fraught with hazards" (1), because the majority of parasites are either eradicated or fail to complete the life cycle. When trypanosomes are ingested by a tsetse fly as part of a blood meal, bloodstream forms differentiate into early procyclic forms in the midgut lumen. In the first few days of tsetse infection, there are two possible outcomes: the parasites are either purged by the fly or they migrate through/around the peritrophic matrix and colonize the ectoperitrophic space. Extraordinarily little is known about this process: teneral (newly hatched) flies are more susceptible to infection, most probably because the peritrophic membrane is not fully formed and it is easier for parasites to gain access to the ectoperitrophic space (2). There is evidence that several hundred parasites from the initial infectious blood meal are founders of the population in the ectoperitrophic space (3). It is not known, however, if these cross the peritrophic matrix individually or if they migrate in groups. The majority of infections in tsetse do not proceed beyond the midgut stage. Completion of the life cycle involves migration of a small number of parasites to the salivary glands, expansion of the founder population as epimastigote forms, and the production of metacyclic forms that can be transmitted to a new mammalian host (1, 3-5).The different life cycle stages of T. brucei in the fly express characteristic glycosylphosphatidylinositol (GPI)-anchored glycoproteins that are present in several million copies per cell and cover the entire surface. The early procyclic forms, which are detected in the fly midgut for up to 7 days following fly infection (6), are characterized by the presence of the GPI-anchor...

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A Glycosylation Mutant of Trypanosoma brucei Links Social Motility Defects In Vitro to Impaired Colonization of Tsetse Flies In Vivo

Imhof

Bütikofer

et al. 2015

Eukaryot Cell

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CELL ADHESION DURING THE MIGRATORY SLUG STAGE OF DICTYOSTELIUM DISCOIDEUM

Bowers-Morrow¹

2002

Cell Biology International

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Prespore-specific Antigen (PsA) is selectively expressed on the surface of prespore cells at the multicellular migratory slug stage of Dictyostelium discoideum development. It is a developmentally regulated glycoprotein that is anchored to the cell membrane through a glycosyl phosphatidylinositol (GPI) anchor. We present the results of an in vitro immunological investigation of the hypothesis that PsA functions as a cell adhesion molecule (CAM), and of a ligand-binding assay indicating that PsA has cell membrane binding partner(s). This is the first evidence to implicate a direct role for a putative CAM in cell-cell adhesion during the multicellular migratory slug stage of D. discoideum development. Cell-cell adhesion assays were carried out in the presence or absence of the monoclonal antibody (mAb) MUD1 that has a single antigenic determinant: a peptide epitope on PsA. These assays showed specific inhibition of cell-cell adhesion by MUD1. Further, it was found that a purified recombinant form of PsA (rPsA), can neutralize the inhibitory effect of MUD1; the inhibitory effect on cell-cell adhesion is primarily due to the blocking of PsA by the mAb. The resistance of aggregates to dissociation in the presence of 10 mM EDTA (ethylenediamintetraacetic acid) indicates that PsA mediates EDTA-stable cell-cell contacts, and that PsA-mediated cell adhesion is likely to be independent of divalent cations such as Ca(2+) or Mg(2+).

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Morphogenetic cell movement in Dictyostelium

Weijer

1999

Seminars in Cell & Developmental Biology

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A monoclonal antibody that interferes with the post‐aggregation adhesion of Dictyostelium discoideum cells

Cited by 4 publications

References 47 publications

A Glycosylation Mutant of Trypanosoma brucei Links Social Motility Defects In Vitro to Impaired Colonization of Tsetse Flies In Vivo

A Glycosylation Mutant of Trypanosoma brucei Links Social Motility Defects In Vitro to Impaired Colonization of Tsetse Flies In Vivo

CELL ADHESION DURING THE MIGRATORY SLUG STAGE OF DICTYOSTELIUM DISCOIDEUM

Morphogenetic cell movement in Dictyostelium

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