@article{BrosterReixFlorimondCayreletal.2021,
  author    = {Broster Reix, Christine E. and Florimond, C{\´e}lia and Cayrel, Anne and Mailh{\´e}, Am{\´e}lie and Agnero-Rigot, Corentin and Landrein, Nicolas and Dacheux, Denis and Havlicek, Katharina and Bonhivers, M{\´e}lanie and Morriswood, Brooke and Robinson, Derrick R.},
  title     = {Bhalin, an essential cytoskeleton-associated protein of Trypanosoma brucei linking TbBILBO1 of the flagellar pocket collar with the hook complex},
  series = {Microorganisms},
  volume    = {9},
  journal   = {Microorganisms},
  number    = {11},
  issn      = {2076-2607},
  doi       = {10.3390/microorganisms9112334},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-250301},
  year      = {2021},
  abstract  = {Background: In most trypanosomes, endo and exocytosis only occur at a unique organelle called the flagellar pocket (FP) and the flagellum exits the cell via the FP. Investigations of essential cytoskeleton-associated structures located at this site have revealed a number of essential proteins. The protein TbBILBO1 is located at the neck of the FP in a structure called the flagellar pocket collar (FPC) and is essential for biogenesis of the FPC and parasite survival. TbMORN1 is a protein that is present on a closely linked structure called the hook complex (HC) and is located anterior to and overlapping the collar. TbMORN1 is essential in the bloodstream form of T. brucei. We now describe the location and function of BHALIN, an essential, new FPC-HC protein. Methodology/Principal Findings: Here, we show that a newly characterised protein, BHALIN (BILBO1 Hook Associated LINker protein), is localised to both the FPC and HC and has a TbBILBO1 binding domain, which was confirmed in vitro. Knockdown of BHALIN by RNAi in the bloodstream form parasites led to cell death, indicating an essential role in cell viability. Conclusions/Significance: Our results demonstrate the essential role of a newly characterised hook complex protein, BHALIN, that influences flagellar pocket organisation and function in bloodstream form T. brucei parasites.},
  language  = {en}
}
@article{SchusterLisackSubotaetal.2021,
  author    = {Schuster, Sarah and Lisack, Jaime and Subota, Ines and Zimmermann, Henriette and Reuter, Christian and Mueller, Tobias and Morriswood, Brooke and Engstler, Markus},
  title     = {Unexpected plasiticty in the life cycle of Trypanosoma brucei},
  series = {eLife},
  volume    = {10},
  journal   = {eLife},
  doi       = {10.7554/eLife.66028.sa2},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-261744},
  year      = {2021},
  abstract  = {African trypanosomes cause sleeping sickness in humans and nagana in cattle. These unicellular parasites are transmitted by the bloodsucking tsetse fly. In the mammalian host's circulation, proliferating slender stage cells differentiate into cell cycle-arrested stumpy stage cells when they reach high population densities. This stage transition is thought to fulfil two main functions: first, it auto-regulates the parasite load in the host; second, the stumpy stage is regarded as the only stage capable of successful vector transmission. Here, we show that proliferating slender stage trypanosomes express the mRNA and protein of a known stumpy stage marker, complete the complex life cycle in the fly as successfully as the stumpy stage, and require only a single parasite for productive infection. These findings suggest a reassessment of the traditional view of the trypanosome life cycle. They may also provide a solution to a long-lasting paradox, namely the successful transmission of parasites in chronic infections, despite low parasitemia.},
  language  = {en}
}
@article{KruegerEngstler2018,
  author    = {Kr{\"u}ger, Timothy and Engstler, Markus},
  title     = {The fantastic voyage of the trypanosome: a protean micromachine perfected during 500 million years of engineering},
  series = {Micromachines},
  volume    = {9},
  journal   = {Micromachines},
  number    = {2},
  doi       = {10.3390/mi9020063},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-175944},
  pages     = {63},
  year      = {2018},
  abstract  = {The human body is constantly attacked by pathogens. Various lines of defence have evolved, among which the immune system is principal. In contrast to most pathogens, the African trypanosomes thrive freely in the blood circulation, where they escape immune destruction by antigenic variation and incessant motility. These unicellular parasites are flagellate microswimmers that also withstand the harsh mechanical forces prevailing in the bloodstream. They undergo complex developmental cycles in the bloodstream and organs of the mammalian host, as well as the disease-transmitting tsetse fly. Each life cycle stage has been shaped by evolution for manoeuvring in distinct microenvironments. Here, we introduce trypanosomes as blueprints for nature-inspired design of trypanobots, micromachines that, in the future, could explore the human body without affecting its physiology. We review cell biological and biophysical aspects of trypanosome motion. While this could provide a basis for the engineering of microbots, their actuation and control still appear more like fiction than science. Here, we discuss potentials and challenges of trypanosome-inspired microswimmer robots.},
  language  = {en}
}