204 research outputs found

    Contrôle moléculaire de la remontée de floraison chez le rosier

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    Rose is a polycarpic plant which presents the ability to flower several times during the year (reccurent blooming. Continuous flowering is due to a mutation of RoKSN a floral repressor homolog to TERMINAL FLOWER 1. In spring, after blooming in once-flowering rose, RoKSN transcripts increase and inhibit nex bloomings. Moreover, the exogenous application of gibberellins (GA) inhibits flowering in spring in once-flowering rose and has no effect on continuous flowering roses. This link between GA and TFL1 was never found before. The main objectives of this study are to understand the function and the regulation of RoKSN and to study the link between RoKSN and GA. By overexpression of RoKSN in Arabidopsis tfl1 mutant we validate floral repressor function of RoKSN. Roses that express ectopically RoKSN, never bloom after few months in greenhouse. In spring exogenous application of GA during floral transition induces RoKSN transcription. The accumulation of RoKSN transcripts correlated with floral inhibition. GA also induces RoFD and Rolfy in a RoKSN-I independent way. To understand the mode of action of RoKS we demonstrate that RoKSN interacted with RoFD. Moreover, there was a competition between RoFT (homologue of FT) and RoKSN FOR RoFD. The consequences of this competition on flowering are still unknow. This study proposed a model for the control of flowering in rose in link with Ga and RoKSN. Other factors as vernalization are under investigation

    Effects of Spatio-Temporal Aliasing on Out-the-Window Visual Systems

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    Designers of out-the-window visual systems face a challenge when attempting to simulate the outside world as viewed from a cockpit. Many methodologies have been developed and adopted to aid in the depiction of particular scene features, or levels of static image detail. However, because aircraft move, it is necessary to also consider the quality of the motion in the simulated visual scene. When motion is introduced in the simulated visual scene, perceptual artifacts can become apparent. A particular artifact related to image motion, spatiotemporal aliasing, will be addressed. The causes of spatio-temporal aliasing will be discussed, and current knowledge regarding the impact of these artifacts on both motion perception and simulator task performance will be reviewed. Methods of reducing the impact of this artifact are also addresse

    Attempts to eradicate two Pelargonium viruses (PFBV and PLPV) by meristem culture and shoot-tip cryotherapy

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    Attempts to eradicate the Pelargonium flower break virus (PFBV) and Pelargonium line pattern virus (PLPV) by meristem culture and apex “droplet-vitrification” cryopreservation was carried out using 5 different cultivars. A simple meristem culture did not permit to eliminate PFBV and only 15% of Pelargonium x hortorum ‘Stellar Artic’ plants regenerated from meristems was PLPV-ELISA-negative. Plants regenerated from cryopreserved apices were tested by DAS-ELISA after a 3-month growing period. Viruses were not detected in 25 and 50% of the tested plants for PFBV and PLPV respectively. Immunolocalisations were carried out for virus localisation in apices from greenhouse plants (control) and vitroplants regenerated after meristem culture or cryopreservation. Immunolocalisations realised on control explants excised from DAS-ELISA positive plants showed that PFBV and PLPV were present in the apices, even in the meristematic dome. However, viral particles were more numerous in the cells of the basal zone than in the more meristematic ones. Immunolocalisations realised on apices from the DAS-ELISA negative cryoregenerated plants showed the viruses were still present. Our results firstly demonstrated that PFBV and PLPV are even present inside meristematic cells and secondly that cryopreservation could decrease their amount in Pelargonium plants but without eliminating them totally. More knowledge on virus behaviour during cryopreservation processes could optimize the management of genetic resources using this conservation method

    Deletion mapping of chromosome 16q in hepatocellular carcinoma

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    Hepatocellular carcinoma (HCC) frequently shows an allelic imbalance (AI) on chromosome 16q. In order to define the commonly affected regions on chromosome 16q, we assessed AI studies in 41 HCCs using a panel of 37 microsatellite markers. Thirty-five cases (85%) showed AI at one or more loci. Among the 35 cases with AI, 21 cases showed multiple AI, suggesting the wide scope of deletion on the long arm of chromosome 16, and the remaining 14 cases showed partial AI. Detailed deletion mapping identified two independent commonly deleted regions on this chromosome arm. These included the D16S3106 locus and D16S498 locus. In conclusion, we have demonstrated frequent AI on 16q in HCCs and identified two loci with frequent AI, which may harbour new tumour suppressor genes.ope

    Mutation analysis of the Fanconi anaemia A gene in breast tumours with loss of heterozygosity at 16q24.3

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    The recently identified Fanconi anaemia A (FAA) gene is located on chromosomal band 16q24.3 within a region that has been frequently reported to show loss of heterozygosity (LOH) in breast cancer. FAA mutation analysis of 19 breast tumours with specific LOH at 16q24.3 was performed. Single-stranded conformational polymorphism (SSCP) analysis on cDNA and genomic DNA, and Southern blotting failed to identify any tumour-specific mutations. Five polymorphisms were identified, but frequencies of occurrence did not deviate from those in a normal control population. Therefore, the FAA gene is not the gene targeted by LOH at 16q24.3 in breast cancer. Another tumour suppressor gene in this chromosomal region remains to be identified. © 1999 Cancer Research Campaig

    Segmentation of corpus callosum using diffusion tensor imaging: validation in patients with glioblastoma

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    Abstract Background This paper presents a three-dimensional (3D) method for segmenting corpus callosum in normal subjects and brain cancer patients with glioblastoma. Methods Nineteen patients with histologically confirmed treatment naïve glioblastoma and eleven normal control subjects underwent DTI on a 3T scanner. Based on the information inherent in diffusion tensors, a similarity measure was proposed and used in the proposed algorithm. In this algorithm, diffusion pattern of corpus callosum was used as prior information. Subsequently, corpus callosum was automatically divided into Witelson subdivisions. We simulated the potential rotation of corpus callosum under tumor pressure and studied the reproducibility of the proposed segmentation method in such cases. Results Dice coefficients, estimated to compare automatic and manual segmentation results for Witelson subdivisions, ranged from 94% to 98% for control subjects and from 81% to 95% for tumor patients, illustrating closeness of automatic and manual segmentations. Studying the effect of corpus callosum rotation by different Euler angles showed that although segmentation results were more sensitive to azimuth and elevation than skew, rotations caused by brain tumors do not have major effects on the segmentation results. Conclusions The proposed method and similarity measure segment corpus callosum by propagating a hyper-surface inside the structure (resulting in high sensitivity), without penetrating into neighboring fiber bundles (resulting in high specificity)

    Topography of the Chimpanzee Corpus Callosum

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    The corpus callosum (CC) is the largest commissural white matter tract in mammalian brains, connecting homotopic and heterotopic regions of the cerebral cortex. Knowledge of the distribution of callosal fibers projecting into specific cortical regions has important implications for understanding the evolution of lateralized structures and functions of the cerebral cortex. No comparisons of CC topography in humans and great apes have yet been conducted. We investigated the topography of the CC in 21 chimpanzees using high-resolution magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI). Tractography was conducted based on fiber assignment by continuous tracking (FACT) algorithm. We expected chimpanzees to display topographical organization similar to humans, especially concerning projections into the frontal cortical regions. Similar to recent studies in humans, tractography identified five clusters of CC fibers projecting into defined cortical regions: prefrontal; premotor and supplementary motor; motor; sensory; parietal, temporal and occipital. Significant differences in fractional anisotropy (FA) were found in callosal regions, with highest FA values in regions projecting to higher-association areas of posterior cortical (including parietal, temporal and occipital cortices) and prefrontal cortical regions (p<0.001). The lowest FA values were seen in regions projecting into motor and sensory cortical areas. Our results indicate chimpanzees display similar topography of the CC as humans, in terms of distribution of callosal projections and microstructure of fibers as determined by anisotropy measures

    Analysis of the 10q23 chromosomal region and the PTEN gene in human sporadic breast carcinoma

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    We examined a panel of sporadic breast carcinomas for loss of heterozygosity (LOH) in a 10-cM interval on chromosome 10 known to encompass the PTEN gene. We detected allele loss in 27 of 70 breast tumour DNAs. Fifteen of these showed loss limited to a subregion of the area studied. The most commonly deleted region was flanked by D10S215 and D10S541 and encompasses the PTEN locus. We used a combination of denaturing gradient gel electrophoresis and single-strand conformation polymorphism analyses to investigate the presence of PTEN mutations in tumours with LOH in this region. We did not detect mutations of PTEN in any of these tumours. Our data show that, in sporadic breast carcinoma, loss of heterozygosity of the PTEN locus is frequent, but mutation of PTEN is not. These results are consistent with loss of another unidentified tumour suppressor in this region in sporadic breast carcinoma. © 1999 Cancer Research Campaig
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