Theodor Staub

Induced Disease Resistance in Plants by Chemicals

Plants can be induced locally and systemically to become more resistant to diseases through various biotic or abiotic stresses. The biological inducers include necrotizing pathogens, non- pathogens or root colonizing bacteria. Through at network of signal pathways they induce resistance spectra and marker proteins that are characteristic for the different plant species and activation systems. The best characterized signal pathway for systemically induced resistance is SAR (systemic acquired resistance) that is activated by localized infections with necrotizing pathogens. It is characterized by protection against a broad range of pathogens, by a set of induced proteins and by its dependence on salicylic acid (SA) Various chemicals have been discovered that seem to act at various points in these defense activating networks and mimic all or parts of the biological activation of resistance. Of these, only few have reached commercialization. The best- studied resistance activator is acibenzolar-5-methyl (BION). At low rates it activates resistance in many crops against a broad spectrum of diseases, including fungi, bacteria and viruses. In monocots, activated resistance by BION typically is very long lasting, while the lasting effect is less pronounced in dicots. BION is translocated systemically in plants and can take the place of SA in the natural SAR signal pathway, inducing the same spectrum of resistance and the same set of molecular markers. Probenazole (ORYZEMATE) is used mainly on rice against rice blast and bacterial leaf blight. Its mode of action is not well understood partly because biological systems of systemically induced resistance are not well defined in rice. Treated plants clearly respond faster and in a resistant manner to infections by the two pathogens. Other compounds like beta-aminobutyric acid as wdl as extracts from plants and microorganisms have also been described as resistance inducers. For most of these, neither the mode of action nor reliable pre-challenge markers are known and still other pathways for resistance activation are suspected. Resistance inducing chemicals that are able to induce broad disease resistance offer an additional option for the farmer to complement genetic disease resistance and the use of fungicides. If integrated properly in plant health management programs, they can prolong the useful life of both the resistance genes and the fungicides presently used.

In vitro selection of sterol-biosynthesis- inhibitor (SBI)-resistant mutants in Monilinia fructicola (Wint.) Honey.

The inherent resistance risk forMonilinia fructicola against sterol-biosynthesis inhibitors (SBIs) was estimated inin vitro andin vivo laboratory studies. Several mutant strains were selected on media amended with the triazole fungicides penconazole, etaconazole or the morpholine fungicide fenpropimorph.The potential forM. fructicola to develop resistance to the triazoles or to the morpholines was similar.The level of resistance attained did not differ for the two classes of fungicides after a single cycle of treatment with nitrosoguanidine (NTG). Attemps to select mutants with a higher level of resistance to penconazole after successive mutagenic treatments were successful. Most of the mutants were less fit than wild-type strains. Mutants with a low level of resistance had an almost normal mycelial growth rate, whereas growth of mutants with a higher level of resistance was significantly reduced. Spore production was highest in the wild-type strains, similar to the latter in a few resistant strains and less in most others. Only one mutant with an intermediate level of resistance could successfully compete in a mixed population with a wild type strain during successive infection cycles on peaches. Resistance was not stable in highly resistant mutants. Cross resistance to the inhibitors of 14-methylsterol demethylation (DMIs) tested was confirmedin vitro andin vivo for all mutant strains. One DMI-resistant mutant was also resistant to fenpropimorph and two fenpropimorph-resistant mutants were resistant to penconazole.SamenvattingOp basis vanin vitro enin vivo laboratoriumstudies werd het risico geschat voor het ontstaan van resistentie-ontwikkeling inMonilinia fructicola tegen sterolbiosynthese remmers (SBIs). Een aantal met nitrosoguanidine (NTG) gemuteerde stammen werd geselecteerd op media met de triazool-fungiciden penconazool, etaconazool of het morfoline-fungicide fenpropimorf.De potentie vanM. fructicola om resistentie te ontwikkelen tegen de triazolen of de morfoline was vergelijkbaar. De resistentiegraad die voor de twee klassen van fungiciden werd gevonden, verschilde niet bij isolaten die na een éénmalige behandeling met NTG werden verkregen. Herhaalde behandeling met NTG leidde tot mutanten met een hogere resistentiegraad voor penconazool. Mutanten met een lage resistentiegraad bezaten een vrijwel normale myceliumgroei, terwijl de groei van mutanten met een relatief hoge resistentiegraad significant lager was. De sporeproduktie van de uitgangsstammen was het hoogst; die van de mutanten was daarmee vergelijkbaar of lager. Slechts één mutant met een middelmatige graad van resistentie vertoonde een competitief vermogen dat vergelijkbaar was met dat van de uitgangsstam. De resistentie in de hoog-resistente mutanten was niet stabiel. Kruisresistentie tegen alle geteste demethyleringsremmers (DMIs) werdin vitro enin vivo bij alle mutanten gevonden. Eén DMI-resistente stam was ook resistent tegen fenpropimorf en twee fenpropimorf-resistente mutanten waren resistent tegen penconazool.