The man-made cereal triticale was fully resistant to the biotrophic diseases powdery mildew, leaf rust, yellow rust, and stem rust from its introduction in Europe in the mid-1970s until about 1990. ...In the following years, new races that were able to infect at least some triticale genotypes developed in all four pathogen populations, and resistance breeding came into focus. Here, we analyzed 656 winter triticale cultivars from 12 countries for resistance to these biotrophic diseases and Fusarium head blight (FHB) at up to 8 location-year combinations (environments). FHB ratings were corrected for plant height and heading stage by comparing three statistical methods. Significant (p < 0.001) genetic variances were found for all resistances with moderate to high entry-mean heritabilities. All traits showed a normal distribution, with the exception of stem rust, where the ratings were skewed towards resistance. There were no substantial correlations among the five disease resistances (r = −0.04 to 0.26). However, several genotypes were detected with multi-disease resistance with a disease rating below average for all five diseases simultaneously. In future, such genotypes must be selected primarily to cope with future challenges of less pesticide use and global climate change.
The following aminopeptidase (AP) activities were found to be associated with the surface of mouse spleen cells: Leu-AP (138 pmol/105 cells×minute) and AP-B (16 pmol/105 cells×minute with ...Lys-β-naphthylamide as substrate and 21 pmol/105 cells×minute with Arg-β-naphthylamide substrate); AP-A activity was not detected by the assay system applied. The immunoactive peptide bestatin inhibited the Leu-AP, while AP-B activity decreased in the presence of both arphamenines A and B and bestatin. No effects on these enzymes were caused by amastatin (an AP-A inhibitor), FK-156, FK-565 and Bu-2743E; the latter peptide turned out to be not an inhibitor of cell surface associated microsomal Leu-AP but an inhibitor of cytosolic Leu-AP. The immunoactive peptides bestatin, arphamenines A and B, and amastatin increased 3Hthymidine incorporation into spleen cells containing lymphocytes and macrophages. These mitogenic actions were not observed when macrophages were removed from the cultures or the cells had been stimulated with ConA or LPS. The lactoyl- and heptanoyl peptides FK-156 and FK-565 caused a mitogenic action on lymphocytes independently of the presence of macrophages. The inhibitor of cytosolic Leu-AP did not change the incorporation into lymphocytes.
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