E leitz wetzlar siemens
However, a pathway for the biosynthesis of IAA without involving Trp has been discovered, where not only IAA, but also high amounts of IAN have been detected ( Normanly et al., 1993). The turnover of indole glucosinolates may provide additional IAN ( Butcher et al., 1974), in particular after tissue disruption during infection with a pathogen or after wounding. It is generally believed that in Brassicaceae the pathway involves the formation of indole-3-acetaldoxime and indole-3-acetonitrile (IAN) from Trp as a precursor ( Ludwig-Müller and Hilgenberg, 1988, 1990, 1992). Several pathways for the biosynthesis of IAA in plants have been discussed ( Normanly et al., 1995). While the vegetative secondary plasmodia of the pathogen produce cytokinins ( Dekhuijzen, 1981 Müller and Hilgenberg, 1986), the increase of indole-3-acetic acid (IAA) might be due to the increased synthesis and turnover of the putative host auxin precursors indole-3-acetaldoxime, indole-3-methylglucosinolate, and indole-3-acetonitrile in infected roots ( Rausch et al., 1981 Searle et al., 1982 Butcher et al., 1984). cytokinins and auxins, are in some way involved in symptom development ( Dekhuijzen and Overeem, 1971 Butcher et al., 1974).
Earlier it was speculated that growth hormones, i.e. leads to cell elongation and cell division in infected roots and hypocotyls, resulting in the typical hypertrophied roots (clubroot) ( Ingram and Tommerup, 1972). The infection of cruciferous hosts with the obligate biotroph Plasmodiophora brassicae Wor. The putative role of nitrilase and auxins during symptom development is discussed. Overexpression of nitrilase did not result in larger clubs compared with the wild type.
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The phenotype of smaller clubs in the mutant was correlated with a lower free indole-3-acetic acid content in the clubs compared with the wild type.
Root galls were smaller in nit1-3 plants compared with the wild type. As a comparison, transgenic plants overexpressing NIT2 under the control of the cauliflower mosaic virus 35S promoter were studied. brassicae infection in a nitrilase mutant ( nit1-3) of Arabidopsis was investigated. To determine which effect a missing nitrilase isoform might have on symptom development, the P. Using a polyclonal antibody against nitrilase, it was shown that the protein was mainly found in infected cells containing sporulating plasmodia, whereas in cells of healthy roots and in uninfected cells of inoculated roots only a few immunosignals were detected. Two peaks of β-glucuronidase activity were visible: an earlier peak (21 d post inoculation) consisting only of the expression of NIT1, and a second peak at about 32 d post inoculation, which predominantly consisted of NIT2 expression.
NIT1 and NIT2 are the nitrilase isoforms predominantly expressed in clubroot tissue, as shown by investigating promoter-β-glucuronidase fusions of each. A time course study showed that only during the exponential growth phase of the clubs was nitrilase prominently enhanced in infected roots compared with controls. The expression of nitrilase in Arabidopsis during the development of the clubroot disease caused by the obligate biotroph Plasmodiophora brassicae was investigated.