Abstract
In vertebrates the microtubule-associated proteins MAP6 and MAP6d1 stabilize cold-resistant microtubules. Cilia and flagella have cold-stable microtubules but MAP6 proteins have not been identified in these organelles. Here, we describe TbSAXO as the first MAP6-related protein to be identified in a protozoan, Trypanosoma brucei. Using a heterologous expression system, we show that TbSAXO is a microtubule stabilizing protein. Furthermore we identify the domains of the protein responsible for microtubule binding and stabilizing and show that they share homologies with the microtubule-stabilizing Mn domains of the MAP6 proteins. We demonstrate, in the flagellated parasite, that TbSAXO is an axonemal protein that plays a role in flagellum motility. Lastly we provide evidence that TbSAXO belongs to a group of MAP6-related proteins (SAXO proteins) present only in ciliated or flagellated organisms ranging from protozoa to mammals. We discuss the potential roles of the SAXO proteins in cilia and flagella function.
Highlights
The cytoskeleton of eukaryotic cells is essential to maintain cell structure and polarization, and to optimize membrane dynamics, intracellular transport, cell division, and locomotion
We have identified TbSAXO as an axonemespecific microtubule-associated proteins (MAPs) protein in the protozoan T. brucei
Knockdown of TbSAXO using RNAiTbSAXO in its natural context reduced flagellar motility suggesting that TbSAXO plays a role in flagellar motility
Summary
The cytoskeleton of eukaryotic cells is essential to maintain cell structure and polarization, and to optimize membrane dynamics, intracellular transport, cell division, and locomotion. MTs are dynamic tubulin polymers where the balance between assembly and disassembly of protofilaments is precisely regulated by microtubule-associated proteins (MAPs) [1]. When phosphorylated, MAP6-1 does not bind to microtubules in vitro and co-localizes with actin filaments in vivo suggesting, as for MAP2c (a mammalian neuronal MAP), a role in neurite initiation [10,11,12]. Map6-null mice exhibit a set of defects similar to those of schizophrenia disorders; the loss of Map is not lethal but is clearly central for normal synaptic plasticity [13]. Taken together, these data indicate a high level of MAP6s regulation
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