26 research outputs found

    Identification and quantification of ‘Candidatus Phytoplasma pyri’ in declining trees of a Swiss cider pear orchard after incision treatment at the stem base

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    Candidatus Orchards of 30 to >100 years old fruit trees used for cider production are endangered by an accumulation of abiotic and biotic stress factors. Among biotic stress factors, diseases such as pear decline (PD) caused by the bacterial pathogen ' Phytoplasma ' contributes to a weakening and reduced life time of affected trees. Since direct treatment of this disease is not possible, approaches have gained attention, which might lead to an increased resilience against this pathogen, such as incisions of the cambium at the graft union at the stem base. Six 35 years old pear trees () of a Swiss cider production orchard, all affected by mild decline were chosen for this study. Four out of them were treated with 2-4 incisions per tree in February 2016. Symptoms were visually assessed during summer and autumn 2016 and 2017, respectively, and ' P ' measured in branch samples with a newly developed duplex TaqMan qPCR assay. No effect could be determined within these two subsequent growing seasons after treatment. Both, visual assessment of symptoms and qPCR measurement of the pathogen in branches did not show any difference between treated and untreated trees. The sequencing of two marker genes of the pathogen detected in this orchard confirmed its identity as ' ' and revealed that it belongs to the major genotype present in Europe

    Drill Milling

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    Dent Disease with Mutations in OCRL1

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    Dent disease is an X-linked renal proximal tubulopathy associated with mutations in the chloride channel gene CLCN5. Lowe syndrome, a multisystem disease characterized by renal tubulopathy, congenital cataracts, and mental retardation, is associated with mutations in the gene OCRL1, which encodes a phosphatidylinositol 4,5-bisphosphate (PIP(2)) 5-phosphatase. Genetic heterogeneity has been suspected in Dent disease, but no other gene for Dent disease has been reported. We studied male probands in 13 families, all of whom met strict criteria for Dent disease but lacked mutations in CLCN5. Linkage analysis in the one large family localized the gene to a candidate region at Xq25-Xq27.1. Sequencing of candidate genes revealed a mutation in the OCRL1 gene. Of the 13 families studied, OCRL1 mutations were found in 5. PIP(2) 5-phosphatase activity was markedly reduced in skin fibroblasts cultured from the probands of these five families, and protein expression, measured by western blotting, was reduced or absent. Slit-lamp examinations performed in childhood or adulthood for all five probands showed normal results. Unlike patients with typical Lowe syndrome, none of these patients had metabolic acidosis. Three of the five probands had mild mental retardation, whereas two had no developmental delay or behavioral disturbance. These findings demonstrate that mutations in OCRL1 can occur with the isolated renal phenotype of Dent disease in patients lacking the cataracts, renal tubular acidosis, and neurological abnormalities that are characteristic of Lowe syndrome. This observation confirms genetic heterogeneity in Dent disease and demonstrates more-extensive phenotypic heterogeneity in Lowe syndrome than was previously appreciated. It establishes that the diagnostic criteria for disorders resulting from mutations in the Lowe syndrome gene OCRL1 need to be revised
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