13 research outputs found

    Reduced tubulin polyglutamylation suppresses flagellar shortness in Chlamydomonas

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    Ciliary length control is an incompletely understood process essential for normal ciliary function. The flagella of Chlamydomonas mutants lacking multiple axonemal dyneins are shorter than normal; previously it was shown that this shortness can be suppressed by the mutation suppressor of shortness 1 (ssh1) via an unknown mechanism. To elucidate this mechanism, we carried out genetic analysis of ssh1 and found that it is a new allele of TPG2 (hereafter tpg2-3), which encodes FAP234 functioning in tubulin polyglutamylation in the axoneme. Similar to the polyglutamylation-deficient mutants tpg1 and tpg2-1, tpg2-3 axonemal tubulin has a greatly reduced level of long polyglutamate side chains. We found that tpg1 and tpg2-1 mutations also promote flagellar elongation in short-flagella mutants, consistent with a polyglutamylation-dependent mechanism of suppression. Double mutants of tpg1 or tpg2-1 and fla10-1, a temperature-sensitive mutant of intraflagellar transport, underwent slower flagellar shortening than fla10-1 at restrictive temperatures, indicating that the rate of tubulin disassembly is decreased in the polyglutamylation-deficient flagella. Moreover, alpha-tubulin incorporation into the flagellar tips in temporary dikaryons was retarded in polyglutamylation-deficient flagella. These results show that polyglutamylation deficiency stabilizes axonemal microtubules, decelerating axonemal disassembly at the flagellar tip and shifting the axonemal assembly/disassembly balance toward assembly

    Epigenetic suppression of mouse Per2 expression in the suprachiasmatic nucleus by the inhalational anesthetic, sevoflurane.

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    BACKGROUND: We previously reported that sevoflurane anesthesia reversibly suppresses the expression of the clock gene, Period2 (Per2), in the mouse suprachiasmatic nucleus (SCN). However, the molecular mechanisms underlying this suppression remain unclear. In this study, we examined the possibility that sevoflurane suppresses Per2 expression via epigenetic modification of the Per2 promoter. METHODS: Mice were anesthetized with a gas mixture of 2.5% sevoflurane/40% oxygen at a 6 L/min flow for 1 or 4 h. After termination, brains were removed and samples of SCN tissue were derived from frozen brain sections. Chromatin immunoprecipitation (ChIP) assays using anti-acetylated-histone antibodies were performed to investigate the effects of sevoflurane on histone acetylation of the Per2 promoter. Interaction between the E'-box (a cis-element in the Per2 promoter) and CLOCK (the Clock gene product) was also assessed by a ChIP assay using an anti-CLOCK antibody. The SCN concentration of nicotinamide adenine dinucleotide (NAD(+)), a CLOCK regulator, was assessed by liquid chromatography-mass spectrometry. RESULTS: Acetylation of histone H4 in the proximal region of the Per2 promoter was significantly reduced by sevoflurane. This change in the epigenetic profile of the Per2 gene was observed prior to suppression of Per2 expression. Simultaneously, a reduction in the CLOCK-E'-box interaction in the Per2 promoter was observed. Sevoflurane treatment did not affect the concentration of NAD(+) in the SCN. CONCLUSIONS: Independent of NAD(+) concentration in the SCN, sevoflurane decreases CLOCK binding to the Per2 promoter E'-box motif, reducing histone acetylation and leading to suppression of Per2 expression

    Complete fusion of a transposon and herpesvirus created the Teratorn mobile element in medaka fish

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    Teratorn is a large mobile genetic element originally identified in the small teleost fish medaka. Here, the authors show that Teratorn is derived from the fusion of a piggyBac superfamily DNA transposon and an alloherpesvirus and that it is widely found across teleost fish

    Changes in histone acetylation at CRE and E’-box in the <i>Per2</i> promoter under sevoflurane anesthesia.

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    <p>(A) Schematic representation of the light/dark condition, sampling periods, and time of anesthetic treatment (gray bar). Arrowheads indicate the time of sampling. (B) Schematic representation of <i>Per2</i> promoter. The positions of primer pairs used for PCR are indicated by arrows. (C, D) Representative PCR results and acetylation levels of histone H3 or H4 at the proximal (C) or distal (D) regions of the <i>Per2</i> promoter. Data are mean ± SEM. * denotes a statistically significant difference between control and anesthetic treatment. † denotes a statistically significant difference between the different time periods of anesthetic exposure (two-way ANOVA followed by Bonferroni test; <i>p</i><0.05).</p

    Suppression of CLOCK binding to the E’-box in the <i>Per2</i> promoter region under sevoflurane anesthesia.

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    <p>The light/dark condition, sampling periods, and time of anesthetic treatment (gray bar) are illustrated in the upper scheme. Arrowheads indicate the time of sampling. Representative PCR results are shown in the middle panel. CLOCK-E’-box binding in each sample is shown in the lower graph. Data are mean ± SEM. * denotes a statistically significant difference between control and anesthetic treatment (Student’s t-test; <i>p</i><0.05).</p

    Inhibition of <i>Per2</i> expression in the SCN under sevoflurane anesthesia.

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    <p>(A) The light/dark conditions and sampling periods are illustrated in the upper scheme. White and black bars indicate light and dark periods, respectively. Arrowheads indicate the time of sampling. Lower graph shows the quantitative diurnal change in <i>Per2</i> expression. (B) The light/dark condition, sampling periods, and time of anesthetic treatment (gray bar) are illustrated in the upper scheme. Changes in <i>Per2</i> expression under anesthetic treatment are shown in the lower graph. Data are mean ± SEM. * denotes a statistically significant difference between anesthetic treatment and control (two-way ANOVA; <i>p</i><0.05).</p

    Le dispositif de VAE militante entre rescolarisation et transformations de l'engagement

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    La validation des acquis de l'expérience (VAE) est un dispositif public créé en 2002, qui permet aux individus d'obtenir des diplômes en faisant reconnaître par des institutions éducatives des activités et des pratiques comme équivalentes aux savoirs et aux savoir-faire acquis dans les formations qui mènent à ces diplômes. La VAE apparaît alors comme un élément de la transformation plus générale de la conception de la formation continue, en ce sens qu'elle met plutôt en scène une conception économiciste, individualiste et instrumentale de la formation, et tout particulièrement parce qu'elle s'appuie sur les deux " outils " socio-cognitifs qui en sont aujourd'hui le cœur : les compétences et le projet. L'étude de la mise en valeur dans les dossiers de VAE des expériences d'engagement montre de quelle manière ce dispositif contribue à développer une conception du militantisme en termes de compétences, en même temps qu'il permet d'insister sur les logiques de rattrapage scolaire qu'il induit
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