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Schwebs, M.

Publications and source records attributed to Schwebs, M..

2 recordsLinked to original sources

Single-molecule fluorescence microscopy demonstrates fast dynamics of the variant surface glycoprotein coat on living trypanosomes

The fluidity of Trypanosoma bruceis dense coat of GPI-anchored variant surface glycoproteins (VSGs) is fundamental for the survival of the parasite. In order to maintain the integrity of the coat, it is recycled on the time scale of a few minutes. This is surprisingly fast as endo- and exocytosis take place in the same small membrane invagination called the flagellar pocket. Here, we present measurements of VSG dynamics on the single-molecule level in living trypanosomes. A large number of short protein trajectories sampling the parasites surface were analysed in two distinct scenarios: diffusion and directed motion. To this end, we employed a previously published algorithm and implemented two extensions to consider rim effects as well as localisations errors inherent to single-mole tracking. Neglect of the latter can have a significant distortive effect on the measured diffusion coefficient; in our case resulting in an underestimation by 20 %. We found large heterogeneity in the local diffusion coefficients and velocities with a surprisingly high average value of [Formula] and [Formula], respectively. To decide on the locally dominant motion mode, we present a guideline based on random walk simulations. We find that VSG dynamics is indeed dominated by diffusion. Complementary simulations on long time scales not accessible in the experiment showed that passive VSG randomisation is fast enough to prevent re-endocytosis newly exocytosed VSGs and to accomplish turnover of the full VSG coat within a few minutes. Author summarySingle-molecule tracking in biological systems often suffers from trajectories being too short to obtain statistically robust decisions on the present motion mode. We faced this issue when investigating the dynamics of the protein surface coat of African trypanosomes. To address the question whether diffusion or directed motion governs coat dynamics, we have adopted an algorithm based on temporal decomposition and spatial binning of an ensemble of single-molecule trajectories. We introduced several extensions to the original approach, including the consideration of localisation errors inherent to single-molecule tracking. This improvement alone already prevented the diffusion coefficient from being underestimated by 20 %. We analysed the coat dynamics in two scenarios, diffusion and directed motion, and offer a decision guideline to identify the locally dominating motion mode. Our extended algorithm is available to the scientific community via GitHub. For the trypanosome surface coat we found that the motion is indeed mainly characterised by diffusion with a surprisingly high diffusion coefficient. This finding solves a long-standing question how the parasite maintains its protein coat.

biophysics↗

Genome maintenance functions of Trypanosoma brucei DNA Polymerase N include telomere association and a role in antigenic variation

Maintenance of genome integrity is critical to guarantee transfer of an intact genome from parent to offspring during cell division. DNA polymerases (Pols) provide roles in both replication of the genome and the repair of a wide range of lesions. Amongst replicative DNA Pols, translesion DNA Pols play a particular role: replication to bypass DNA damage, often at the cost of mutation. All cells express a range of translesion Pols, but little work has examined their function in parasites, including whether the enzymes might contribute to host-parasite interactions. Here, we describe a dual function of translesion PolN in African trypanosomes. Previously we demonstrated that PolN is associated with telomeric sequences and now we show that RNAi-mediated depletion of PolN results in slowed growth, altered DNA content, changes in cell morphology, and increased sensitivity to DNA damaging agents. Depletion of PolN leads to chromosome segregation defects and accumulation of DNA damage. We also show that PolN displays discrete localisation at the nuclear periphery in the absence of exogenous DNA damage. In addition, we demonstrate that PolN depletion leads to deregulation of telomeric variant surface glycoprotein genes, linking the function of this translesion DNA polymerase to host immune evasion by antigenic variation.

microbiology↗