
Microtubule polyglutamylation is important for regulating cytoskeletal architecture and motility in Trypanosoma brucei
Author(s) -
Jana Jentzsch,
Adal Sabri,
Konstantin Speckner,
Gertrud Lallinger-Kube,
Matthias Weiß,
Klaus Ersfeld
Publication year - 2020
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.248047
Subject(s) - biology , trypanosoma brucei , cytoskeleton , microbiology and biotechnology , microtubule , tubulin , motility , axoneme , cell division , cell , biochemistry , flagellum , gene
The shape of kinetoplastids, such as Trypanosoma brucei, is precisely defined during the stages of the life cycle and governed by a stable subpellicular microtubule cytoskeleton. During the cell cycle and transitions between life cycle stages this stability has to transiently give way to a dynamic behaviour to enable cell division and morphological rearrangements. How these opposing requirements of the cytoskeleton are regulated is poorly understood. Two possible levels of regulation are activities of cytoskeleton-associated proteins and microtubule posttranslational modifications (PTMs). Here, we investigate the functions of two putative tubulin polyglutamylases in T. brucei, TTLL6A and TTLL12B. Depletion of both proteins leads to a reduction in tubulin polyglutamylation in situ and is associated with disintegration of the posterior cell pole, loss of the microtubule plus end-binding protein EB1 and alterations of microtubule dynamics. We also observe a reduced polyglutamylation of the flagellar axoneme. Quantitative motility analysis reveals that the PTM disbalance correlates with a transition from directional to diffusive cell movement. These data show, that microtubule polyglutamylation has an important role in regulating cytoskeletal architecture and motility in this parasite.