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PubMed1989

Ca2+/calmodulin-dependent phosphorylation of ciliary beta-tubulin in Tetrahymena.

The ciliary axoneme is the minimal structure responsible for Ca2+-dependent modulation of ciliary movement. We demonstrated that, in Tetrahymena ciliary axonemes, beta-tubulin was exclusively phosphorylated by an endogenous Ca2+/calmodulin-dependent protein kinase(s). The phosphorylation of beta-tubulin also occurred in the outerdoublet microtubule fraction, suggesting that the responsible enzyme(s) was tightly associated with outerciliary motility, Ca2+-dependent phosphorylation of beta-tubulin was also found to occur exclusively. From these results, it is inferable that the phosphorylation of beta-tubulin is involved in Ca2+-dependent ciliary reversal.

Animals↗
PubMed1995

Tubulin stimulates adenylyl cyclase activity in rat striatal membranes via transfer of guanine nucleotide to Gs protein.

Previous studies of rat cerebral cortex and rat C6 glioma cells have demonstrated that dimeric tubulin is capable of activating the G proteins Gs and Gil via transfer of guanine nucleotide from tubulin to Gs alpha and Gil alpha. To provide further information regarding cytoskeletal modulation of adenylyl cyclase, the present study examined effects of tubulin on the activation of the enzyme in rat striatal membranes. Tubulin, prepared from rat brain by polymerization with the hydrolysis-resistant GTP analog 5'-guanylylimidodiphosphate (GppNHp) caused significant activation of adenylyl cyclase by approximately 130%. Furthermore, tubulin-GppNHp activated SKF 38393-sensitive adenylyl cyclase and potentiated forskolin-stimulated activity of the enzyme. When tubulin, polymerized with the hydrolysis-resistant photoaffinity GTP analog [32p]p3 (4-azidoanilido)-p1-5'-GTP ([32P]AAGTP), was incubated with striatal membranes, AAGTP was transferred from tubulin to Gs alpha as well as Gi alpha with the extents of nucleotide transfers being 7.6 +/- 0.8% and 17.8 +/- 1.4% of AAGTP originally bound to tubulin, respectively. These results indicate that, in rat striatum, the tubulin dimer participates in the stimulatory regulation of adenylyl cyclase by transferring guanine nucleotide to Gs alpha, supporting the hypothesis that tubulin contributes to the regulation of neuronal signal transduction.

Adenylyl Cyclases↗
PubMed2002

Selective enhanced phosphorylation of shrimp beta-tubulin by PKC-delta with PEP(taxol), a synthetic peptide encoding the taxol binding region.

Beta-tubulin cDNA from the shrimp Penaeus japonicus was isolated by homology cloning. Expression of cDNA in Escherichia coli yielded a 55 kDa polypeptide, positive for monoclonal antibodies against mammalian beta-tubulin. Autoradiography demonstrated the bacterially expressed hepatopancreas beta-tubulin of P. japonicus is specifically phosphorylated by the delta isoenzyme of protein kinase C (PKC-delta) purified from the plasma membrane of the shrimp heart, in the presence of the receptor for activated PKC (RACK), but not in its absence. Purified shrimp heart PKC-delta is able to phosphorylate bacterially expressed shrimp beta-tubulin without the presence of Ca(++), but requires Mg(++). The kinase activity of purified PKC-delta on bacterially expressed beta-tubulin was enhanced by incubation with PEP(taxol), a synthetic peptide encoding the taxol-binding region of beta-tubulin. In other words, PEP(taxol) modulates the kinase activity of PKC-delta through RACK.

Amino Acid Sequence↗
PubMed1992

Brain microtubule-associated proteins modulate microtubule dynamic instability in vitro. Real-time observations using video microscopy.

We used video assays to study the dynamic instability behavior of individual microtubules assembled in vitro with purified tau, purified MAP2 or a preparation of unfractionated heat-stable MAPs. Axoneme-nucleated microtubules were assembled from pure tubulin at concentrations between 4 and 9 microM in the presence of MAPs, and observed by video-differential interference contrast microscopy. Microtubules co-assembled with each MAP preparation exhibited the elongation and rapid shortening phases and the abrupt transitions (catastrophe and rescue) characteristic of dynamic instability. Each MAP preparation increased the microtubule elongation rate above that for purified tubulin alone by decreasing the tubulin subunit dissociation rate during elongation. The brain MAPs used in this study reduced the rate of microtubule rapid shortening, but allowed significant loss of polymer during the shortening phase. Purified tau and MAP2 decreased the frequency of catastrophe and increased the frequency of rescue, while the heat-stable MAPs suppressed catastrophe at all but the lowest tubulin concentrations. Thus, each of these MAPs modulates, but does not abolish, dynamic instability behavior of microtubules. We propose a model to explain how MAP2 and tau bind to the microtubule lattice at sites along protofilaments so that the MAPs promote polymerization, but do not significantly block the mechanism of rapid shortening inherent in the tubulin lattice. Rapid shortening, when it occurs, proceeds primarily by the dissociation of short fragments of protofilaments, which contain the bound MAPs.

Animals↗
PubMed2005

Three- and four-repeat tau regulate the dynamic instability of two distinct microtubule subpopulations in qualitatively different manners. Implications for neurodegeneration.

The microtubule-associated protein tau is implicated in the pathogenesis of many neurodegenerative diseases, including fronto-temporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), in which both RNA splicing and amino acid substitution mutations in tau cause dominantly inherited early onset dementia. RNA-splicing FTDP-17 mutations alter the wild-type approximately 50:50 3-repeat (3R) to 4-repeat (4R) tau isoform ratio, usually resulting in an excess of 4R tau. To examine further how splicing mutations might cause dysfunction by misregulation of microtubule dynamics, we used video microscopy to determine the in vitro behavior of individual microtubules stabilized by varying amounts of human 4R and 3R tau. At low tau:tubulin ratios (1:55 and 1:45), all 3R isoforms reduced microtubule growth rates relative to the no-tau control, whereas all 4R isoforms increased them; however, at a high tau:tubulin ratio (1:20), both 4R and 3R tau increased the growth rates. Further analysis revealed two distinct subpopulations of growing microtubules in the absence of tau. Increasing concentrations of both 4R and 3R tau resulted in an increase in the size of the faster growing subpopulation of microtubules; however, 4R tau caused a redistribution to the faster growing subpopulation at lower tau:tubulin ratios than 3R tau. This modulation of discrete growth rate subpopulations by tau suggests that tau causes a conformational shift in the microtubule resulting in altered dynamics. Quantitative and qualitative differences observed between 4R and 3R tau are consistent with a "microtubule misregulation" model in which abnormal tau isoform expression results in the inability to properly regulate microtubule dynamics, leading to neuronal death and dementia.

Alternative Splicing↗
PubMed1998

P-glycoprotein is more efficient at limiting uptake than inducing efflux of colchicine and vinblastine in HL-60 cells.

PURPOSE: To investigate the role of the P-glycoprotein (P-gp) drug efflux pump in the intracellular disposition of colchicine and vinblastine. METHODS: Uptake and efflux kinetics were studied in vitro in human lymphocytes and in HL-60 cells with or without the P-gp modulator, verapamil. RESULTS: In human lymphocytes, colchicine was slowly taken up (uptake half-life was 18.9+/-1.1 hr.) and verapamil increased colchicine uptake by 37%, whereas it did not modify colchicine efflux from cells. In HL-60 cells, colchicine uptake was non-linear and slower than that of vinblastine, the colchicine uptake half-life (11.1+/-0.5 hr.) being 25-fold longer than that of vinblastine at 25 nM. Verapamil did not significantly modify colchicine uptake half-life, but increased its intracellular accumulation by 23% and that of vinblastine by 81%. Immuno-flow cytometry showed that P-gp expression in HL-60 cells increased significantly from 24 hr. following colchicine or vinblastine exposure. The significant increase in colchicine uptake induced by verapamil at 24 hr. was correlated with this enhanced P-gp expression. The drug efflux half-life was 11.5-fold higher for colchicine (23+/-0.9 hr) than vinblastine, indicating a much slower elimination of colchicine from cells that could be related to its longer dissociation half-life from the tubulin receptor. Verapamil treatment did not modulate either colchicine or vinblastine efflux kinetics, suggesting that the intracellular drugs are not available to the transmembrane P-gp binding sites. CONCLUSIONS: P-gp may not be the main reason for the slowness of colchicine uptake. It may be more efficient at controlling entry of colchicine and vinblastine through the plasma membrane than at mediating their efflux from HL-60 cells.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Inhibitors of kinesin Eg5: antiproliferative activity of monastrol analogues against human glioblastoma cells.

The inhibition of kinesin Eg5 by small molecules such as monastrol is currently evaluated as an approach to develop a novel class of antiproliferative drugs for the treatment of malignant tumours. Therefore, we studied the effects of the new monastrol analogues enastron, dimethylenastron and vasastrol VS-83 on the proliferation of human glioblastoma cells in the kinetic crystal violet assay. Compared to monastrol, the new cell cycle specific compounds showed an at least one order of magnitude higher anti proliferative activity against U-87 MG, U-118 MG, and U-373 MG glioblastoma cells. The compounds were neither inactivated by hydrolysis nor by binding to serum proteins. Moreover, we demonstrated the characteristic monoaster formation after incubation of cells with the new compounds by confocal laser scanning microscopy. We also showed that the arrangement of beta-actin and tubulin, vital components of the cyto-skeleton of mitotic and quiescent cells, were not affected by the new compounds. Due to the necessity of overcoming the blood-brain barrier in the treatment of brain tumours, we investigated if the new monastrol analogues are modulators or substrates of the p-glycoprotein (p-gp) 170 by a flow cytometric calcein-AM efflux assay. The tested compounds showed no modulating effects on the p-gp function. With respect to the treatment of primary and secondary CNS tumours, the results of our experiments suggest that the new monastrol analogues represent an interesting class of potential anticancer drugs, predicted to be less neurotoxic in comparison to classical tubulin inhibitors.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

Role of the carboxy terminal region of beta tubulin on microtubule dynamics through its interaction with the GTP phosphate binding region.

The dynamic instability of microtubules depends on the GTP binding to tubulin, the rate of hydrolysis of GTP bound to tubulin molecules, at the microtubule caps, and on the affinity and exchange rate of tubulin for GTP versus GDP. It has been demonstrated that the binding of microtubule-associated proteins (MAPs) such as Tau or MAP2 notably enhances microtubule stability in vivo. These MAPs bind to the tubulin carboxy terminal domain. Consequently, an attractive hypothesis to explain the modulation of microtubule dynamics by MAPs is that the carboxy terminal domain of tubulin interacts with a region close to the GTP binding site, preventing the binding of GTP or exchange of GDP for GTP. By carrying out a combined analysis of crosslinking and limited proteolysis, an intramolecular interaction between the carboxy terminus and the tubulin region containing the GTP binding site in beta tubulin has been observed. It is proposed that this interaction modifies the binding of GTP to the tubulin beta-subunit and, therefore, affects tubulin assembly dynamics. This suggests a molecular explanation for the effect of MAPs in facilitating tubulin polymerization through the regulation of the interaction of GTP.

Amino Acid Sequence↗
PubMed1988

Laser-transected microtubules exhibit individuality of regrowth, however most free new ends of the microtubules are stable.

To study the possible mechanism of microtubule turnover in interphase cells, we have used the 266-nm wavelength of a short-pulsed Nd/YAG laser to transect microtubules in situ in PtK2 cells at predefined regions. The regrowth and shrinkage of the transected microtubules have been examined by staining the treated cells with antitubulin mAb at various time points after laser irradiation. The results demonstrate that microtubules grow back into the transected zones individually; neither simultaneous growth nor shrinkage of all microtubules has been observed. The half-time of replacement of laser-dissociated microtubules is observed to be approximately 10 min. On the other hand, exposure of the core of the microtubule, which is expected to consist almost completely of GDP-tubulin, by transecting the internal regions of the microtubule does not render the remaining polymer catastrophically disassembled, and most transected microtubules with free minus ends do not quickly disappear. Taken together, these results suggest that most microtubules in cultured interphase cells exhibit some properties of dynamic instability (individual regrowth or shrinkage); however, other factors in addition to the hydrolysis of GTP-tubulin need to be involved in modulating the dynamics and the stability of these cytoplasmic microtubules.

Animals↗
PubMed2003

The role of Ppe1/PP6 phosphatase for equal chromosome segregation in fission yeast kinetochore.

Mis12 is a kinetochore protein essential for equal chromosome segregation and is evolutionarily conserved from yeast to human. In this study, we report the isolation and characterization of suppressors of the mis12 mutant in fission yeast. Our results indicate that Mis12 is negatively regulated by a highly conserved protein phosphatase Ppe1 (scSit4/dmPPV/hPP6) or its bound partner Ekc1 (scSAP), and it is positively regulated by a counteracting kinase Gsk3. Mass spectrometry analysis shows that at least two sites in Mis12 are phosphorylated. This mechanism of suppression occurs at the level of localization recovery of Mis12 to the kinetochore chromatin. Consistently, Mis12 and a subpopulation of Ppe1/Ekc1 were found to behave like non-histone-type chromatin-associating proteins in the chromatin fractionation assay. Mutant analysis of Ppe1 and Ekc1 revealed that they are important for faithful chromosome segregation, as the mutants exhibited unequal chromosome segregation similar to mis12 in the presence of a low concentration of tubulin poison. Ppe1/PP6 directly or indirectly modulates kinetochore chromatin protein Mis12 to ensure progression into normal anaphase.

Amino Acid Sequence↗
PubMed1994

Low doses of neutrons induce changes in gene expression.

Studies were designed to identify genes induced in fibroblasts after exposure to low-dose neutron radiation but not after gamma rays. Our past work had shown similar modulation of transcripts for alpha-tubulin, beta- and gamma-actins, ornithine decarboxylase and interleukin 1 after exposure to either neutrons or gamma rays. However, differences in the expression of beta-protein kinase C and c-fos genes were observed, with both being induced after exposure to gamma rays but not neutrons. Recently we have identified two genes that are induced after exposure to neutrons but not gamma rays: Rp-8 (a gene associated with apoptosis) and the long terminal repeat (LTR) of the human immunodeficiency virus (HIV). Induction of Rp-8 mRNA was demonstrated in Syrian hamster embryo (SHE) fibroblasts and was found to be induced in cells exposed to neutrons administered at low (0.005 Gy/min) and high dose rate (0.12 Gy/min). No induction of other genes associated with apoptosis such as Rp-2, bcl-2 and Tcl-30 was observed. The induction of transcription from the LTR of HIV was demonstrated in HeLa cells bearing a transfected construct of the chloramphenicol acetyl transferase (CAT) gene driven by the HIV-LTR promoter. Measurements of CAT activity and CAT transcripts after irradiation demonstrated an unresponsiveness to gamma rays over a broad range of doses (0.1-3 Gy). Twofold induction of the HIV-LTR was detected after exposure to neutrons (0.48 Gy) administered at low (0.05 Gy/min) but not high (0.12 Gy/min) dose rates. Ultraviolet-mediated HIV-LTR induction, however, was inhibited by exposure to low-dose-rate neutron irradiation. These results are interesting in light of reports that Rp-8 is induced during apoptosis and that HIV causes apoptosis.

Animals↗
PubMedDate not supplied

Metastasis associated MTS1 and NM23 genes affect tubulin polymerisation in B16 melanomas: a possible mechanism of their regulation of metastatic behaviour of tumours.

The nm23 and mts1 genes are associated with the expression of the metastatic phenotype. We have shown previously that modulation of metastatic behaviour produces parallel changes in the expression of these genes and that the expression of the two genes is co-regulated. Here we show that modulation of gene expression affects the process of tubulin polymerisation. B16 melanoma cell lines F1 and ML8 were treated with alpha melanocyte stimulating hormone (MSH) and all-trans retinoic acid (RA) respectively. MSH reduced the proportion of nm23+ and increased mts1+ F1 cells, with a 55% decrease in the ratio nm23:mts1. In parallel, MSH increased the expression of depolymerised form of tubulin in these cells. Treatment of ML8 cells with RA decreased mts1 positivity to a greater extent that nm23 positivity and the nm23:mts1 ratio increased by 70% and, in parallel, reduced the expression of depolymerised form of tubulin. These data suggest that nm23 and mts1 gene expression regulates the biological behaviour of the tumour cell and confer on it invasive and metastasizing properties by affecting the state of tubulin polymerisation.

Animals↗
PubMed2002

Cloning and characterization of the 5'-flanking region of the rat neuron-specific Class III beta-tubulin gene.

The promoter regions of several neuron-specific structural proteins (e.g. neurofilaments, peripherin, Talpha1-tubulin) have revealed potential regulatory elements that could contribute to the choice of a neuronal phenotype during development. We initiated study of the 5'-flanking region of the rat Class III neuron-specific beta-tubulin gene (betaIII-tubulin) because this gene is expressed at the time of terminal mitosis only in neurons and thus its promoter should be an excellent tool for studying neuron-specific gene expression during the transition from proliferative progenitor cell to early neuronal differentiation. We identified the minimal promoter region needed to drive expression of the betaIII-tubulin gene. This minimal region contains multiple putative binding sites for the transcription factors SP1 and AP2, as well as a central nervous system enhancer regulatory element and an E-box. A primer extension analysis identifies a single transcription start site. We highlight several putative regulatory elements that may modulate the expression of the betaIII-tubulin gene in a stage- and tissue-specific manner. In addition, we show that the first 490 bp of the promoter are sufficient to regulate betaIII-tubulin gene expression during neuronal differentiation of PCC7 cells.

5' Flanking Region↗
PubMed1984

Identification of the major postsynaptic density protein as homologous with the major calmodulin-binding subunit of a calmodulin-dependent protein kinase.

The major postsynaptic density protein (mPSDp), comprising greater than 50% of postsynaptic density (PSD) protein, is an endogenous substrate for calmodulin-dependent phosphorylation as well as a calmodulin-binding protein in PSD preparations. The results in this investigation indicate that mPSDp is highly homologous with the major calmodulin-binding subunit (p) of tubulin-associated calmodulin-dependent kinase (TACK), and that PSD fractions also contain a protein homologous with the sigma-subunit of TACK. Homologies between mPSDp and a 63,000 dalton PSD protein and the rho- and sigma-subunits of TACK were established by the following criteria: (1) identical apparent molecular weights; (2) identical calmodulin-binding properties; (3) manifestation of Ca2+-calmodulin-stimulated autophosphorylation; (4) identical isoelectric points; (5) identical calmodulin binding and autophosphorylation patterns on two-dimensional gels; (6) homologous two-dimensional tryptic peptide maps; and (7) similar phosphoamino acid-specific phosphorylation of tubulin. The results suggest that mPSDp is a calmodulin-binding protein involved in modulating protein kinase activity in the postsynaptic density and that a tubulin kinase system homologous with TACK exists in a membrane-bound form in the PSD.

Animals↗
PubMed1997

Dimeric tubulin-stimulated adenylyl cyclase activity is augmented after long-term amitriptyline treatment.

We have investigated altered association of tubulin dimers interacting with G proteins and modulating adenylyl cyclase (AC) as a result of long-term amitriptyline (AMT) treatment. Gpp(NH)p-stimulated, but not basal or manganese-stimulated, AC activity was significantly augmented in cortex membranes prepared from rats chronically treated with AMT. The enhancement of AC activity by Gpp(NH)p-liganded tubulin (tubulin-Gpp(NH)p) was significantly higher in chronically AMT-treated rats than in control rats. Moreover, in cortex membranes from controls, tubulin-Gpp(NH)p prepared from chronically AMT-treated rats was more effective to activate AC activity than tubulin-Gpp(NH)p from controls. Immunoblotting and photoaffinity guanine nucleotide binding procedures showed no significant differences in the amount and the function of G proteins between controls and AMT-treated groups. It is suggested that long-term AMT treatment causes alteration in the functional interaction between tubulin and G protein, and this modification may participate in enhanced coupling of Gs to the catalytic subunit of AC induced by the chronic antidepressant treatment.

Adenylyl Cyclases↗
PubMed1997

Coassembly of bovine and cod microtubule proteins: the ratio of the different tubulins within hybrid microtubules determines the ability to assemble at low temperatures, MAPs dependency and effects of Ca2+.

Cod and bovine microtubule proteins (MTP) differ from each other in many respects, e.g., tubulin isoforms and microtubule-associated proteins (MAPs) but only cod MTP are cold-adapted. We used these differences to determine how tubulin isoform composition affects microtubule properties. Mixtures of cod and bovine MTP coassembled at 30 degrees C as shown by light scattering and immunoelectron microscopy, with no apparent preference for one set of MAPs over the other. Bovine tubulin was, in contrast to cod tubulin, unable to assemble in the absence of MAPs, while 50%/50% mixtures of bovine and cod tubulin, respectively, coassembled readily without exclusion of cod or bovine tubulin isoforms in the hybrids, as shown by two-dimensional gel electrophoresis. Alteration in MAPs dependency was also confirmed by the use of the MAPs-binding microtubule inhibitor estramustine phosphate. Addition of 10 mM Ca2+ to microtubules induced formation of spirals or rings depending on the ratio of the cod and bovine MTP, respectively. Bovine MTP were unable to assemble at low temperatures, while cod MTP are cold-adapted and assembled efficiently at 14 degrees C in the presence of MAPs. Amounts of cod MTP as low as 33% were enough to induce assembly of bovine/cod MTP hybrids. The critical concentration for assembly of a 50%/50% mixture was similar to that of 100% cod MTP. Taken together, the results show that the divergent cod and bovine MTP can coassemble, and that alterations in tubulin isotype/isoform composition above certain thresholds significantly modulate microtubule properties such as MAPs dependency, effects of Ca2+, and ability to assemble at low temperatures.

Adaptation, Physiological↗
PubMed1986

Tubulin isotypes: generation of diversity in cells and microtubular organelles.

Diversity of tubulin isotypes is illustrated by consideration of the beta-tubulin isotypes of higher plants and the eukaryotic microbe, Physarum polycephalum, and by the alpha-tubulin isotypes of the protozoan, Trypanosoma brucei. The carrot plant expresses six, well-defined beta-tubulin isotypes that possess characteristic two-dimensional gel coordinates. These six beta-tubulin isotypes are differentially expressed during development of the flowering plant. In a similar manner, Physarum expresses three separate beta-tubuli isotypes during its life cycle; of the two beta 1 isotypes, one is expressed solely in the myxamoeba whilst the other is expressed both in the myxamoeba and in the plasmodium. A further beta-tubulin isotype, beta 2, is expressed only in the plasmodium. In carrot and in Physarum the generation of beta-tubulin diversity appears, in the main, to be generated by the differential expression of a beta-tubulin multi-gene family. However, tubulin isotypes can also be generated by post-translational modifications and T. brucei utilizes two different modifications within one cell. First, the primary translation product, the alpha 1-tubulin isotype, can be acetylated to produce the alpha 3 isotype. Second, both the alpha 1 and alpha 3 isotypes appear to exist in both tyrosinated and detyrosinated forms. The generation of these alpha-tubulin isotypes within the same cell and their presence in particular cellular domains, modulated throughout the cell cycle, reveals a complex relationship between alpha-tubulin isotypes produced by post-translational modifications and the dynamics of microtubule construction.

Animals↗
PubMed2007

Zinc and the cytoskeleton in the neuronal modulation of transcription factor NFAT.

Transcription factor NFAT is crucial in the development of the nervous system due to its role in neuronal plasticity and survival. In this study we characterized the role of zinc and the cytoskeleton in the modulation of NFAT in neuronal cells. The incubation of cells in zinc deficient media led to NFAT activation that was inhibited by the calcium chelator BAPTA and the antioxidants (+/-)-alpha-lipoic acid and N-acetyl cysteine, suggesting the involvement of calcium and oxidants in the initial steps of NFAT activation associated with zinc deficiency. At a second step of regulation, a decrease in cellular zinc led to an impaired transport of the active NFAT from the cytosol into the nucleus due to alterations in tubulin polymerization secondary to a decrease in neuronal zinc. Furthermore, disruption of the cytoskeleton structure by cold and chemical agents (colchicine (Col), vinblastine (VB), cytochalasin D (Cyt)) also inhibited NFAT transport into the nucleus. The altered nuclear transport caused a decrease in NFAT-dependent gene expression. This study demonstrates for the first time that zinc can modulate transcription factor NFAT in neuronal cells, and that microtubules are involved in NFAT nuclear translocation, crucial event in the regulation of NFAT transcriptional activity.

Active Transport, Cell Nucleus↗