Tubulin modifications and their cellular functions

Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Current Opinion in Cell Biology (Impact Factor: 8.47). 03/2008; 20(1):71-6. DOI: 10.1016/
Source: PubMed


All microtubules are built from a basic alpha/beta-tubulin building block, yet subpopulations of microtubules can be differentially marked by a number of post-translational modifications. These modifications, conserved throughout evolution, are thought to act individually or in combination to control specific microtubule-based functions, analogous to how histone modifications regulate chromatin functions. Here we review recent studies demonstrating that tubulin modifications influence microtubule-associated proteins such as severing proteins, plus-end tracking proteins, and molecular motors. In this way, tubulin modifications play an important role in regulating microtubule properties, such as stability and structure, as well as microtubule-based functions, such as ciliary beating, cell division, and intracellular trafficking.

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    • "The various post-translational modifications including: acetylation, palmitoylation, tyrosination/detyrosination, glutamylation, and glycylation help to co-regulate ciliary stability and motility232425. The acetylation of microtubules is the most frequent post-translational modification associated with microtubule stabilization [26]. However, it is believed that that this modification does not directly increase stability [25,27]. "
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    ABSTRACT: Cilia and flagella are evolutionarily conserved, membrane-bound, microtubule-based organelles on the surface of most eukaryotic cells. They play important roles in coordinating a variety of signaling pathways during growth, development, cell mobility, and tissue homeostasis. Defects in ciliary structure or function are associated with multiple human disorders called ciliopathies. These diseases affect diverse tissues, including, but not limited to the eyes, kidneys, brain, and lungs. Many processes must be coordinated simultaneously in order to initiate ciliogenesis. These include cell cycle, vesicular trafficking, and axonemal extension. Centrioles play a central role in both cell cycle progression and ciliogenesis, making the transition between basal bodies and mitotic spindle organizers integral to both processes. The maturation of centrioles involves a functional shift from cell division toward cilium nucleation which takes place concurrently with its migration and fusion to the plasma membrane. Several proteinaceous structures of the distal appendages in mother centrioles are required for this docking process. Ciliary assembly and maintenance requires a precise balance between two indispensable processes; so called assembly and disassembly. The interplay between them determines the length of the resulting cilia. These processes require a highly conserved transport system to provide the necessary substances at the tips of the cilia and to recycle ciliary turnover products to the base using a based microtubule intraflagellar transport (IFT) system. In this review; we discuss the stages of ciliogenesis as well as mechanisms controlling the lengths of assembled cilia.
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    • "We therefore tested the effects of Kif26b on MT stabilization. It has been reported that stable MTs, as compared to dynamic MTs, accumulate more modifications (Hammond et al., 2008). Acetylated-tubulin, a post translational modification of tubulin, has been reported to protect MT from depolymerization and thus may reinforce MT stability (Kaverina and Straube, 2011). "
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    ABSTRACT: Angiogenesis involves the coordinated growth and migration of endothelial cells (EC) toward a proangiogenic signal. The Wnt Planar Cell Polarity (PCP) pathway, through the recruitment of Dishevelled (Dvl) and Dvl associated activator of morphogenesis (Daam1), has been proposed to regulate cell actin cytoskeleton and microtubule (MT) reorganization for oriented cell migration. Here, we report that Kif26b, a kinesin, and Daam1 cooperatively regulate initiation of EC sprouting and directional migration via MT reorganization. First, we found that Kif26b is recruited within the Dvl3/Daam1 complex. Using a 3D in vitro angiogenesis assay, we showed that Kif26b and Daam1 depletion impairs tip cell polarization and destabilizes extended vascular processes. Kif26b depletion specifically alters EC directional migration and mislocalized MT-Organizing Center (MTOC)/Golgi and Myosin IIB cell rear enrichment, therefore the cell fails to establish a proper front-rear polarity. Interestingly, Kif26b ectopic expression rescues the siDaam1 polarization defect phenotype. Finally, we highlighted that Kif26b functions on MT stabilization, which is indispensable for asymmetrical cell structure reorganization. These data demonstrate that Kif26b together with Dvl3/Daam1 initiates cell polarity through the control of PCP signaling pathway-dependent activation.
    Preview · Article · Jan 2016 · Molecular Biology of the Cell
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    • "It is well known that the basic resistance mechanism of fungal species to fungicides is due to a modification at the target-site of fungicidal action (Brent and Hollomon 1998). The interrelationships of carbendazim resistance with point mutations of the β-tubulin gene have been analyzed in details (Verhey and Gaetig 2007; Hammond et al. 2008; Cheng et al. 2009). Many studies have shown that the mechanism of action for carbendazim fungicides is binding to β-tubulin and preventing α-tubulin assembly (Fujimura et al. 1992; Cools et al. 2011; Cools and Fraaije 2012). "
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    ABSTRACT: The application of fungicides is so critical, especially in greenhouses, to avoid fungal infections. Carbendazim, an inhibitor of tubulin biosynthesis, is the most widely known broad-spectrum benzimidazole fungicide. The application of carbendazim affects other beneficial fungi as well. Paecilomyces lilacinus 36-1 (Pl36-1) is a beneficial fungus used for biological control, and the most effective biocontrol agents of nematode eggs. The Pl36-1 is sensitive to carbendazim (0.3 μg/ml). There is a general consensus that the mechanisms of resistance to carbendazim in the β-tubulin gene have been analyzed in detail. However, no studies were conducted on P. lilacinus strains. In the present study, two carbendazim-resistant mutants of Pl36-1, P50 and P100, were obtained from UV exposure and tested. The β-tubulin gene fragments were cloned and sequenced in the three strains, Pl36-1, P50 and P100. The resistance to carbendazim was developed when amino acid substitutions occurred at β-tubulin gene positions of S145A, T185A and F200Y. The β-tubulin gene was overexpressed in Pl36-1 strains. The β-tubulin expression level of the overexpressed mutant (PL3), quantified by qRT-PCR, was increased 4-folds over its normal level in Pl36-1. In vitro, the PL3 was resistant to carbendazim with maintaining growth, sporulation and pathogenicity rates. Three-year field trial demonstrated that P100 and PL3 strains exhibited carbendazim resistance combined with high nematode reduction and yield improvement.
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