Refine
Has Fulltext
- yes (7)
Is part of the Bibliography
- yes (7)
Document Type
- Journal article (7)
Language
- English (7)
Keywords
- cell surface (2)
- African trypanosome (1)
- African trypanosomes (1)
- GPI-anchor (1)
- Kinetoplastea (1)
- RNA (1)
- Rab (1)
- Trypanosoma (1)
- bilayers (1)
- binding (1)
- brucei (1)
- cell cycle and cell division (1)
- cell differentiation (1)
- cell surface proteome (1)
- cellular imaging (1)
- clathrin (1)
- cloning (1)
- depth (1)
- endocytosis (1)
- environment (1)
- evolution (1)
- exocytosis (1)
- host-pathogen interaction (1)
- hyperexpression techniques (1)
- immune epitope mapping (1)
- infection (1)
- membrane biophysics (1)
- membrane fission (1)
- membrane recycling (1)
- nanotube formation (1)
- nanovesicle formation (1)
- parasite evolution (1)
- parasite genetics (1)
- parasitic cell cycles (1)
- parasitic diseases (1)
- parasitology (1)
- probes (1)
- protein (1)
- protein crowding (1)
- signal peptides (1)
- single-molecule biophysics (1)
- structural biology (1)
- tetracyclines (1)
- trypanosome lytic factor (1)
- variant surface glycoproteins (1)
Institute
For persistent infections of the mammalian host, African trypanosomes limit their population size by quorum sensing of the parasite-excreted stumpy induction factor (SIF), which induces development to the tsetse-infective stumpy stage. We found that besides this cell density-dependent mechanism, there exists a second path to the stumpy stage that is linked to antigenic variation, the main instrument of parasite virulence. The expression of a second variant surface glycoprotein (VSG) leads to transcriptional attenuation of the VSG expression site (ES) and immediate development to tsetse fly infective stumpy parasites. This path is independent of SIF and solely controlled by the transcriptional status of the ES. In pleomorphic trypanosomes varying degrees of ES-attenuation result in phenotypic plasticity. While full ES-attenuation causes irreversible stumpy development, milder attenuation may open a time window for rescuing an unsuccessful antigenic switch, a scenario that so far has not been considered as important for parasite survival.