Academic literature on the topic 'Mobilité flagellaire'

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Journal articles on the topic "Mobilité flagellaire"

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Soares, Maurilio J., Reginaldo P. Brazil, Amilcar Tanuri, and Wanderley de Souza. "Some ultrastructural aspects of Crithidia guilhermei n.sp. isolated from Phaenicia cuprina (Diptera: Calliphoridae)." Canadian Journal of Zoology 64, no. 12 (December 1, 1986): 2837–42. http://dx.doi.org/10.1139/z86-408.

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A flagellate trypanosomatid was isolated from the fly Phaenicia cuprina captured in Rio de Janeiro, Brazil. It grows well in liver infusion – trypticase medium, in the form of choanomastigotes, typical of the genus Crithidia. Morphometrical data obtained at the light microscopical level indicated that the new isolated Crithidia is smaller than Crithidia luciliae, a parasite isolated from Phaenicia sericata. Transmission electron microscopy of thin sections revealed that this trypanosomatid has a flagellar pocket divided into two compartments, one basal and the other apical, separated by a region of attachment of the flagellum to the cell body. The attachment region was characterized in freeze-fracture replicas. The flagellate has a compact kinetoplast DNA network. As in endosymbiote-containing trypanosomatids previously described, no subpellicular microtubules were seen in the regions where the mitochondria touched the plasma membrane, although no endosymbiotes were found in this flagellate. Electrophoretic mobility of six enzymes showed that the parasite could not be grouped in any of the isoenzymic pattern groups of other Crithidia spp. These observations indicate that the trypanosomatid isolated from P. cuprina is a new species of Crithidia. The flagellate is described as Crithidia guilhermei n.sp.
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Harris, J. Aaron, Yi Liu, Pinfen Yang, Peter Kner, and Karl F. Lechtreck. "Single-particle imaging reveals intraflagellar transport–independent transport and accumulation of EB1 in Chlamydomonas flagella." Molecular Biology of the Cell 27, no. 2 (January 15, 2016): 295–307. http://dx.doi.org/10.1091/mbc.e15-08-0608.

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The microtubule (MT) plus-end tracking protein EB1 is present at the tips of cilia and flagella; end-binding protein 1 (EB1) remains at the tip during flagellar shortening and in the absence of intraflagellar transport (IFT), the predominant protein transport system in flagella. To investigate how EB1 accumulates at the flagellar tip, we used in vivo imaging of fluorescent protein–tagged EB1 (EB1-FP) in Chlamydomonas reinhardtii. After photobleaching, the EB1 signal at the flagellar tip recovered within minutes, indicating an exchange with unbleached EB1 entering the flagella from the cell body. EB1 moved independent of IFT trains, and EB1-FP recovery did not require the IFT pathway. Single-particle imaging showed that EB1-FP is highly mobile along the flagellar shaft and displays a markedly reduced mobility near the flagellar tip. Individual EB1-FP particles dwelled for several seconds near the flagellar tip, suggesting the presence of stable EB1 binding sites. In simulations, the two distinct phases of EB1 mobility are sufficient to explain its accumulation at the tip. We propose that proteins uniformly distributed throughout the cytoplasm like EB1 accumulate locally by diffusion and capture; IFT, in contrast, might be required to transport proteins against cellular concentration gradients into or out of cilia.
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Ko, Minsu, and Chankyu Park. "H-NS-Dependent Regulation of Flagellar Synthesis Is Mediated by a LysR Family Protein." Journal of Bacteriology 182, no. 16 (August 15, 2000): 4670–72. http://dx.doi.org/10.1128/jb.182.16.4670-4672.2000.

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ABSTRACT H-NS regulates the flagellar master operon (flhDC) and thus is necessary for flagellation of Escherichia coli. However, the molecular mechanism of its regulation has remained unknown. Genetic screening of a transposon insertion abolishing the H-NS effect revealed a previously unidentified gene, namedhdfR, encoding a LysR family protein. Binding of purified HdfR to the flhDC promoter was demonstrated by a DNA mobility shift assay, indicating that HdfR is a transcriptional regulator for the flagellar master operon. Furthermore, the expression of the hdfR gene was shown to be negatively regulated by H-NS.
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Correa, Nidia E., and Karl E. Klose. "Characterization of Enhancer Binding by the Vibrio cholerae Flagellar Regulatory Protein FlrC." Journal of Bacteriology 187, no. 9 (May 1, 2005): 3158–70. http://dx.doi.org/10.1128/jb.187.9.3158-3170.2005.

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ABSTRACT The human pathogen Vibrio cholerae is a highly motile organism by virtue of a polar flagellum, and motility has been inferred to be an important aspect of virulence. It has previously been demonstrated that the σ54-dependent activator FlrC is necessary for both flagellar synthesis and for enhanced intestinal colonization. In order to characterize FlrC binding, we analyzed two FlrC-dependent promoters, the highly transcribed flaA promoter and the weakly transcribed flgK promoter, utilizing transcriptional lacZ fusions, mobility shift assays, and DNase I footprinting. Promoter fusion studies showed that the smallest fragment with wild-type transcriptional activity for flaAp was from positions −54 to +137 with respect to the start site, and from −63 to +144 for flgKp. Gel mobility shift assays indicated that FlrC binds to a fragment containing the region from positions +24 to +95 in the flaAp, and DNase I footprinting identified a protected region between positions +24 and +85. Mobility shift and DNase I footprinting indicated weak binding of FlrC to a region downstream of the flgKp transcription start site. These results demonstrate a relatively novel σ54-dependent promoter architecture, with the activator FlrC binding downstream of the σ54-dependent transcription start sites. When the FlrC binding site(s) in the flaA promoter was moved a large distance (285 bp) upstream of the transcription start site of either flaAp or flgKp, high levels of FlrC-dependent transcription resulted, indicating that this binding region functions as an enhancer element. In contrast, the relatively weak FlrC binding site(s) in the flgK promoter failed to function as an enhancer element at either promoter, suggesting that FlrC binding strength contributes to enhancer activity. Our results suggest that the differences in FlrC binding to various flagellar promoters results in the differences in transcription levels that mirror the relative requirement for the flagellar components within the flagellum.
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Teplitski, Max, Robert I. Goodier, and Brian M. M. Ahmer. "Pathways Leading from BarA/SirA to Motility andVirulence Gene Expression inSalmonella." Journal of Bacteriology 185, no. 24 (December 15, 2003): 7257–65. http://dx.doi.org/10.1128/jb.185.24.7257-7265.2003.

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ABSTRACT The barA and sirA genes of Salmonella enterica serovar Typhimurium encode a two-component sensor kinase and a response regulator, respectively. This system increases the expression of virulence genes and decreases the expression of motility genes. In this study, we examined the pathways by which SirA affects these genes. We found that the master regulator of flagellar genes, flhDC, had a positive regulatory effect on the primary regulator of intestinal virulence determinants, hilA, but that hilA had no effect on flhDC. SirA was able to repress flhDC in a hilA mutant and activate hilA in an flhDC mutant. Therefore, although the flhDC and hilA regulatory cascades interact, sirA affects each of them independently. A form of BarA lacking the two N-terminal membrane-spanning domains, BarA198, autophosphorylates in the presence of ATP and transfers the phosphate to purified SirA. Phosphorylated SirA was found to directly bind the hilA and hilC promoters in gel mobility shift assays but not the flhD, fliA, hilD, and invF promoters. Given that the CsrA/csrB system is known to directly affect flagellar gene expression, we tested the hypothesis that SirA affects flagellar gene expression indirectly by regulating csrA or csrB. The sirA gene did not regulate csrA but did activate csrB expression. Consistent with these results, phosphorylated SirA was found to directly bind the csrB promoter but not the csrA promoter. We propose a model in which SirA directly activates virulence expression via hilA and hilC while repressing the flagellar regulon indirectly via csrB.
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Soscia, Chantal, Abderrahman Hachani, Alain Bernadac, Alain Filloux, and Sophie Bleves. "Cross Talk between Type III Secretion and Flagellar Assembly Systems in Pseudomonas aeruginosa." Journal of Bacteriology 189, no. 8 (February 16, 2007): 3124–32. http://dx.doi.org/10.1128/jb.01677-06.

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ABSTRACT Pseudomonas aeruginosa cytotoxicity is linked to a type III secretion system (T3SS) that delivers effectors into the host cell. We show here that a negative cross-control exists between T3SS and flagellar assembly. We observed that, in a strain lacking flagella, T3SS gene expression, effector secretion, and cytotoxicity were increased. Conversely, we revealed that flagellar-gene expression and motility were decreased in a strain overproducing ExsA, the T3SS master regulator. Interestingly, a nonmotile strain lacking the flagellar filament (ΔfliC) presented a hyperefficient T3SS and a nonmotile strain assembling flagella (ΔmotAB) did not. More intriguingly, a strain lacking motCD genes is a flagellated strain with a slight defect in swimming. However, in this strain, T3SS gene expression was up-regulated. These results suggest that flagellar assembly and/or mobility antagonizes the T3SS and that a negative cross talk exists between these two systems. An illustration of this is the visualization by electron microscopy of T3SS needles in a nonmotile P. aeruginosa strain, needles which otherwise are not detected. The molecular basis of the cross talk is complex and remains to be elucidated, but proteins like MotCD might have a crucial role in signaling between the two processes. In addition, we found that the GacA response regulator negatively affects the T3SS. In a gacA mutant, the T3SS effector ExoS is hypersecreted. Strikingly, GacA was previously reported as a positive regulator for motility. Globally, our data document the idea that some virulence factors are coordinately but inversely regulated, depending on the bacterial colonization phase and infection types.
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Jian, Huahua, Guanpeng Xu, Yingbao Gai, Jun Xu, and Xiang Xiao. "The Histone-Like Nucleoid Structuring Protein (H-NS) Is a Negative Regulator of the Lateral Flagellar System in the Deep-Sea Bacterium Shewanella piezotolerans WP3." Applied and Environmental Microbiology 82, no. 8 (February 12, 2016): 2388–98. http://dx.doi.org/10.1128/aem.00297-16.

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ABSTRACTAlthough the histone-like nucleoid structuring protein (H-NS) is well known for its involvement in the adaptation of mesophilic bacteria, such asEscherichia coli, to cold environments and high-pressure stress, an understanding of the role of H-NS in the cold-adapted benthic microorganisms that live in the deep-sea ecosystem, which covers approximately 60% of the earth's surface, is still lacking. In this study, we characterized the function of H-NS inShewanella piezotoleransWP3, which was isolated from West Pacific sediment at a depth of 1,914 m. Anhnsgene deletion mutant (WP3Δhns) was constructed, and comparative whole-genome microarray analysis was performed. H-NS had a significant influence (fold change, >2) on the expression of a variety of WP3 genes (274 and 280 genes were upregulated and downregulated, respectively), particularly genes related to energy production and conversion. Notably, WP3Δhnsexhibited higher expression levels of lateral flagellar genes than WP3 and showed enhanced swarming motility and lateral flagellar production compared to those of WP3. The DNA gel mobility shift experiment showed that H-NS bound specifically to the promoter of lateral flagellar genes. Moreover, the high-affinity binding sequences of H-NS were identified by DNase I protection footprinting, and the results support the “binding and spreading” model for H-NS functioning. To our knowledge, this is the first attempt to characterize the function of the universal regulator H-NS in a deep-sea bacterium. Our data revealed that H-NS has a novel function as a repressor of the expression of genes related to the energy-consuming secondary flagellar system and to swarming motility.
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Williams, B. D., D. R. Mitchell, and J. L. Rosenbaum. "Molecular cloning and expression of flagellar radial spoke and dynein genes of Chlamydomonas." Journal of Cell Biology 103, no. 1 (July 1, 1986): 1–11. http://dx.doi.org/10.1083/jcb.103.1.1.

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Several flagellar dynein ATPase and radial spokehead genes have been isolated from a Chlamydomonas genomic expression library in lambda gt11. The library was probed with polyclonal and monoclonal antibodies raised against purified flagellar polypeptides, and recombinant phage giving positive signals were cloned. In vitro translation of mRNAs hybrid-selected by the cloned sequences from whole cell RNA provided confirmation of identity for three of the four clones. Evidence supporting the identification of the fourth, which encodes a dynein heavy chain, was provided by antibody selection; the fusion protein produced by this clone selected heavy chain-specific antibodies from a complex polyclonal antiserum recognizing many dynein determinants. One of the radial spoke sequences isolated here is of particular interest because it encodes the wild-type allele of a locus which was defined previously by temperature-sensitive paralyzed flagella mutation pf-26ts (Huang, B., G. Piperno, Z. Ramanis, and D. J. L. Luck, 1981, J. Cell Biol., 88:80-88). The cloned sequence was used to hybrid-select mRNA from mutant pf-26ts cells, and when translated in vitro, the selected mRNA produced a mutant spokehead polypeptide with an altered electrophoretic mobility. This confirms that the pf-26ts mutation alters the primary structure of a radial spokehead polypeptide. To quantify spokehead and dynein mRNAs during flagellar regeneration, all of the cloned sequences were used as hybridization probes in RNA dot experiments. Levels increased rapidly and coordinately after deflagellation, peaked 3-10-fold above nondeflagellated controls, and then returned to control values within 2 h. This accumulation pattern was similar to that of flagellar alpha-tubulin mRNA.
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Wen, Yi, Jing Feng, David R. Scott, Elizabeth A. Marcus, and George Sachs. "The pH-Responsive Regulon of HP0244 (FlgS), the Cytoplasmic Histidine Kinase of Helicobacter pylori." Journal of Bacteriology 191, no. 2 (October 31, 2008): 449–60. http://dx.doi.org/10.1128/jb.01219-08.

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ABSTRACT Helicobacter pylori colonizes the acidic gastric environment, in contrast to all other neutralophiles, whose acid resistance and tolerance responses allow only gastric transit. This acid adaptation is dependent on regulation of gene expression in response to pH changes in the periplasm and cytoplasm. The cytoplasmic histidine kinase, HP0244, which until now was thought only to regulate flagellar gene expression via its cognate response regulator, HP0703, was found to generate a response to declining medium pH. Although not required for survival at pH 4.5, HP0244 is required for survival at pH 2.5 with 10 mM urea after 30 min. Transcriptional profiling of a HP0244 deletion mutant grown at pH 7.4 confirmed the contribution of HP0244 to σ54 activation via HP0703 to coordinate flagellar biosynthesis by a pH-independent regulon that includes 14 flagellar genes. Microarray analysis of cells grown at pH 4.5 without urea revealed an additional 22 genes, including 4 acid acclimation genes (ureA, ureB, ureI, and amiE) that are positively regulated by HP0244. Additionally, 86 differentially expressed genes, including 3 acid acclimation genes (ureF, rocF [arginase], and ansB [asparaginase]), were found in cells grown at pH 2.5 with 30 mM urea. Hence, HP0244 has, in addition to the pH-independent flagellar regulon, a pH-dependent regulon, which allows adaptation to a wider range of environmental acid conditions. An acid survival study using an HP0703 mutant and an electrophoretic mobility shift assay with in vitro-phosphorylated HP0703 showed that HP0703 does not contribute to acid survival and does not bind to the promoter regions of several genes in the HP0244 pH-dependent regulon, suggesting that there is a pathway outside the HP0703 regulon which transduces the acid-responsive signal sensed by HP0244.
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Kim, Yun-Kyeong, and Linda L. McCarter. "ScrG, a GGDEF-EAL Protein, Participates in Regulating Swarming and Sticking in Vibrio parahaemolyticus." Journal of Bacteriology 189, no. 11 (March 30, 2007): 4094–107. http://dx.doi.org/10.1128/jb.01510-06.

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ABSTRACT In this work, we describe a new gene controlling lateral flagellar gene expression. The gene encodes ScrG, a protein containing GGDEF and EAL domains. This is the second GGDEF-EAL-encoding locus determined to be involved in the regulation of swarming: the first was previously characterized and named scrABC (for “swarming and capsular polysaccharide regulation”). GGDEF and EAL domain-containing proteins participate in the synthesis and degradation of the nucleotide signal cyclic di-GMP (c-di-GMP) in many bacteria. Overexpression of scrG was sufficient to induce lateral flagellar gene expression in liquid, decrease biofilm formation, decrease cps gene expression, and suppress the ΔscrABC phenotype. Removal of its EAL domain reversed ScrG activity, converting ScrG to an inhibitor of swarming and activator of cps expression. Overexpression of scrG decreased the intensity of a 32P-labeled nucleotide spot comigrating with c-di-GMP standard, whereas overexpression of scrG Δ EAL enhanced the intensity of the spot. Mutants with defects in scrG showed altered swarming and lateral flagellin production and colony morphology (but not swimming motility); furthermore, mutation of two GGDEF-EAL-encoding loci (scrG and scrABC) produced cumulative effects on swarming, lateral flagellar gene expression, lateral flagellin production and colony morphology. Mutant analysis supports the assignment of the primary in vivo activity of ScrG to acting as a phosphodiesterase. The data are consistent with a model in which multiple GGDEF-EAL proteins can influence the cellular nucleotide pool: a low concentration of c-di-GMP favors surface mobility, whereas high levels of this nucleotide promote a more adhesive Vibrio parahaemolyticus cell type.
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Dissertations / Theses on the topic "Mobilité flagellaire"

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Indiana, Arnaud. "Rôles du chimiotactisme et de la mobilité flagellaire dans la fitness des Xanthomonas." Thesis, Angers, 2014. http://www.theses.fr/2014ANGE0009/document.

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Les bactéries du genre xanthomonas sont responsables de nombreuses maladies des plantes, telles que la nervation noire des brassicacées causée par x. campestris pv. campestris (xcc). Lors des phases précoces du processus infectieux, ces bactéries doivent identifier des sites favorables à leur pénétration dans les tissus et les atteindre afin de s'internaliser dans les tissus végétaux et s’y multiplier. Le chimiotactisme est le mécanisme par lequel les bactéries détectent des signaux et se dirigent vers des attractants ou s’éloignent de signaux répulsifs. L’objectif de ce travail est de comprendre les rôles du chimiotactisme et de la mobilité flagellaire dans la fitness des xanthomonas. Nous avons montré que la mobilité flagellaire n’est pas une caractéristique partagée par tous les xanthomonas mais qu’environ 5% des souches perdent cette capacité sans altération majeure de leur fitness in planta. Un senseur du chimiotactisme, dénommé hsb1, probablement acquis par transfert horizontal, présente un groupe d’allèles spécifique à x. campestris. Une mutation de hsb1 dans la souche xcc atcc 33913 entraine une diminution de l’internalisation de cette souche dans les tissus de plantes hôtes combinée à une augmentation de l’internalisation dans les tissus des plantes non-hôtes. Hsb1 perçoit un signal émis par les blessures des feuilles de chou. Un glucosinolate, la sinigrine, et un acide aminé, la l-phénylalanine, sont détectés in vitro par ce senseur, mais ne sont pas métabolisés. Des travaux complémentaires seront nécessaires pour identifier le signal détecté par ce senseur et envisager la conception de méthodes de lutte basées sur la confusion d’informations
Xanthomonads are responsible for plant diseases such as black rot of Brassicaceae caused by X. campestris pv. campestris (Xcc). During the early stages of the infection, pathogenic bacteria such as Xcc must detect favorable sites and ingress into host plant tissues to colonize and multiply in the apoplast or the xylem vessels. Chemotaxis is the mechanism used by bacteria to detect attractants and repellents and adapt in consequence its direction. The aim of this work is to understand the roles of chemotaxis and flagellar motility in the fitness of xanthomonads. We showed that flagellar motility is not a general feature of xanthomonads. About 5 % of tested strains lost this ability without major impact on their fitness in planta. A chemotaxis sensor, named Hsb1, probably acquired by horizontal transfer shows a group of alleles that are specific of X. campestris. In Xcc ATCC 33913, a mutation in hsb1 resulted in a decreased penetration of this strain in the host plant tissues combined with an increase penetration in the non-host plant tissues. Hsb1 sense a signal from wounds of cabbage leaves. In vitro, a glucosinolate, the sinigrin, and an amino acid, the L-phenylalanine are detected by Hsb1 but are not metabolized. Further work is needed to identify the signal detected by the sensor and to design control methods based on confusion
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Demonchy, Raphaël. "Etude de protéines flagellaires chez Trypanosoma brucei." Paris 6, 2008. http://www.theses.fr/2008PA066294.

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Les flagelles sont des organites conservés dans le monde eucaryote. Chez l’Homme ils sont présents dans un grand nombre de types cellulaires et leur disfonctionnement est la cause de maladies graves. La conservation des protéines est telle qu’il est possible, par comparaison de génomes, d’établir des ensembles de gènes flagellaires putatifs. Trypanosoma brucei est un protiste parasite qui possède un flagelle mobile tout au long de son cycle biologique. Avec ce modèle d’étude, nous avons confirmé le rôle dans la mobilité flagellaire de quatre protéines conservées dans les espèces possédant des flagelles mobiles, dont l’hydine, protéine impliquée dans l’hydrocéphalie. D’autre part nous avons travaillé sur deux protéines de la famille 9 des kinésines : TbKLP1 et TbKIF9. Les deux kinésines sont flagellaires et impliquées dans la mobilité. TbKIF9, elle, est nécessaire pour l’assemblage de la fibre paraflagellaire (PFR), la structure associée à l’axonème du trypanosome. Des structures extra-axonémales sont aussi présentes dans les spermatozoïdes, et il s’agit de la première démonstration du rôle d’une kinésine dans l’assemblage de telles structures
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BERREBBAH, HOURIA. "Etude du controle de la mobilite flagellaire et ciliaire par le calcium. Effet du lindane, insecticide organochlore." Paris 7, 1990. http://www.theses.fr/1990PA077177.

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Le travail presente dans cette these concerne l'analyse du battement ciliaire et le role des ions calcium dans la regulation de cette activite. L'effet d'un insecticide organochlore, le lindane, connu pour son effet cilio-inhibiteur a egalement ete aborde. Le materiel biologique utilise est un protiste eucaryote sans paroi: dunaliella. Cette algue est mobile grace a deux cils situes au niveau de son pole anterieur. Elle est cultivee dans des conditions parfaitement controlees permettant d'etudier les consequences des modifications de l'environnement sur son mouvement. L'etude du mouvement ciliaire de dunaliella a ete abordee par deux methodes quantitatives, la microcinematographie suivie du traitement d'images et la velocimetrie doppler laser. Les resultats obtenus montrent que la vitesse de deplacement de l'algue ne depend pas de la concentration externe en calcium. En effet, apres un sejour de 15 jours dans un milieu sans calcium, l'algue conserve son mouvement. Ceci suggere l'existence de reserves calciques intracellulaires importantes. L'analyse par une sonde aux rayons x, confirme cette hypothese. Le lindane provoque une inhibition rapide et dose-dependante du battement ciliaire. Cet effet specifique du lindane, se retrouve egalement sur le battement flagellaire de spermatozoide de rat. Grace a des preparations de dunaliella, demembranees et reactivees, nous avons pu montrer que le lindane n'a pas d'action directe sur l'axoneme. Les etudes des flux et efflux de calcium radioactif ont montre que cet insecticide n'a aucun effet sur la sortie de calcium alors qu'il en inhibe fortement l'entree. L'analyse du cycle des phosphoinositides indique par contre que le lindane qui est un analogue du myoinositol, ne semble pas affecter ce cycle. Ces resultats nous ont conduit a formuler l'hypothese selon laquelle le mouvement ciliaire est dependant de la concentration intracellulaire en calcium et que le lindane
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