9 research outputs found

    Stereotactic body radiation therapy for a new lung cancer arising after pneumonectomy: dosimetric evaluation and pulmonary toxicity

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    To evaluate the tolerance of stereotactic body radiation therapy (SBRT) for the treatment of secondary lung tumours in patients who underwent previous pneumonectomy

    Historical Introgression of the Downy Mildew Resistance Gene Rpv12 from the Asian Species Vitis amurensis into Grapevine Varieties

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    The Amur grape (Vitis amurensis Rupr.) thrives naturally in cool climates of Northeast Asia. Resistance against the introduced pathogen Plasmopara viticola is common among wild ecotypes that were propagated from Manchuria into Chinese vineyards or collected by Soviet botanists in Siberia, and used for the introgression of resistance into wine grapes (Vitis vinifera L.). A QTL analysis revealed a dominant gene Rpv12 that explained 79% of the phenotypic variance for downy mildew resistance and was inherited independently of other resistance genes. A Mendelian component of resistance\u2013a hypersensitive response in leaves challenged with P. viticola\u2013was mapped in an interval of 0.2 cM containing an array of coiled-coil NB-LRR genes on chromosome 14. We sequenced 10-kb genic regions in the Rpv12+ haplotype and identified polymorphisms in 12 varieties of V. vinifera using next-generation sequencing. The combination of two SNPs in single-copy genes flanking the NB-LRR cluster distinguished the resistant haplotype from all others found in 200 accessions of V. vinifera, V. amurensis, and V. amurensis x V. vinifera crosses. The Rpv12+ haplotype is shared by 15 varieties, the most ancestral of which are the century-old \u2018Zarja severa\u2019 and \u2018Michurinets\u2019. Before this knowledge, the chromosome segment around Rpv12+ became introgressed, shortened, and pyramided with another downy mildew resistance gene from North American grapevines (Rpv3) only by phenotypic selection. Rpv12+ has an additive effect with Rpv3+ to protect vines against natural infections, and confers foliar resistance to strains that are virulent on Rpv3+ plant

    Historical Introgression of the Downy Mildew Resistance Gene <i>Rpv12</i> from the Asian Species <i>Vitis amurensis</i> into Grapevine Varieties

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    <div><p>The Amur grape (<i>Vitis amurensis</i> Rupr.) thrives naturally in cool climates of Northeast Asia. Resistance against the introduced pathogen <i>Plasmopara viticola</i> is common among wild ecotypes that were propagated from Manchuria into Chinese vineyards or collected by Soviet botanists in Siberia, and used for the introgression of resistance into wine grapes (<i>Vitis vinifera</i> L.). A QTL analysis revealed a dominant gene <i>Rpv12</i> that explained 79% of the phenotypic variance for downy mildew resistance and was inherited independently of other resistance genes. A Mendelian component of resistance–a hypersensitive response in leaves challenged with <i>P. viticola</i>–was mapped in an interval of 0.2 cM containing an array of coiled-coil NB-LRR genes on chromosome 14. We sequenced 10-kb genic regions in the <i>Rpv12<sup>+</sup></i> haplotype and identified polymorphisms in 12 varieties of <i>V. vinifera</i> using next-generation sequencing. The combination of two SNPs in single-copy genes flanking the NB-LRR cluster distinguished the resistant haplotype from all others found in 200 accessions of <i>V. vinifera</i>, <i>V. amurensis</i>, and <i>V. amurensis</i> x <i>V. vinifera</i> crosses. The <i>Rpv12<sup>+</sup></i> haplotype is shared by 15 varieties, the most ancestral of which are the century-old ‘Zarja severa’ and ‘Michurinets’. Before this knowledge, the chromosome segment around <i>Rpv12<sup>+</sup></i> became introgressed, shortened, and pyramided with another downy mildew resistance gene from North American grapevines (<i>Rpv3</i>) only by phenotypic selection. <i>Rpv12<sup>+</sup></i> has an additive effect with <i>Rpv3<sup>+</sup></i> to protect vines against natural infections, and confers foliar resistance to strains that are virulent on <i>Rpv3<sup>+</sup></i> plants.</p> </div

    Host–pathogen interaction observed between host and pathogen genotypes.

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    <p>Leaf discs of four host genotypes including (panels <b>A</b>, <b>E</b>) a double homozygous recessive grapevine (<i>Rpv12<sup>−</sup></i> and <i>Rpv3<sup>−</sup></i>), (panels <b>B</b>, <b>F</b>) a grapevine carrying <i>Rpv3<sup>+</sup></i> in the absence of <i>Rpv12<sup>+</sup></i>, (panels <b>C</b>, <b>G</b>) a grapevine carrying <i>Rpv12<sup>+</sup></i> in the absence of <i>Rpv3<sup>+</sup></i>, and (panels <b>D</b>, <b>H</b>) a double heterozygous grapevine for both <i>Rpv12<sup>+</sup></i> and <i>Rpv3<sup>+</sup></i> were inoculated with two isolates of <i>P. viticola</i>, (panels <b>A</b>–<b>D</b>) <i>Rude</i> (<i>avrRpv3<sup>+</sup></i>/<i>avrRpv12<sup>+</sup></i>) and (panels <b>E</b>–<b>H</b>) <i>Pv127</i> (<i>avrRpv3<sup>−</sup></i>/<i>avrRpv12<sup>+</sup></i>). Pictures were taken at 6 dpi.</p

    Phenotypic distribution of downy mildew resistance.

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    <p>Two families segregating for <i>Rpv12<sup>+</sup></i> (panel <b>A</b>) and for the combination of <i>Rpv12<sup>+</sup></i> and <i>Rpv3<sup>+</sup></i> (panel <b>B</b>) were analysed. Resistance scores in panel <b>A</b> are based on the OIV452 parameter (1 = most sensitive, 9 = most resistant) scored on field-grown seedlings under natural infection. Resistance scores in panel <b>B</b> are based on the cumulative OIV452 parameter (∑OIV452 = sum of daily OIV452 scores from 3 to 8 dpi) in artificially inoculated leaf discs. The average phenotypic value in the upper left corner of the panels <b>A</b>–<b>B</b> refers to individuals grouped by their allelic status at the <i>Rpv12</i> and <i>Rpv3</i> genes, which was estimated based on the flanking markers UDV014/UDV370 for <i>Rpv12</i>, and on UDV305/UDV737 for <i>Rpv3 </i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0061228#pone.0061228-DiGaspero1" target="_blank">[8]</a>. Recombinants in those intervals were excluded from this estimate. QTL plots that explain the phenotypic variance shown in panel <b>B</b> are given in panel <b>C</b>.</p
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