The biotrophic powdery mildew fungus Blumeria graminis releases extracellular materials to the surface of fungal infection structures that facilitate anchoring them to hydrophobic plant surfaces prior to infection; however, the chemistry of fungal adhesives and the mechanism of adhesion remain largely unclear. Expressed sequence tag analysis led to identification of a secreted lipase, Lip1, from B. graminis. Expression of LIP1 is dramatically upregulated during the early stages of fungal development. Lip1, secreted to the surface of fungal cell walls, possesses lipolytic activity against a broad range of glycerides and releases alkanes and primary fatty alcohols from the epicuticular wax of wheat leaves. Of the epicuticular wax components released by Lip1 activity, long-chain alkanes are the most efficient cues for triggering appressorium formation. Pretreatment of wheat leaves with Lip1, thereby removing leaf surface wax, severely compromises components of fungal pathogenicity, including conidial adhesion, appressorium formation, and secondary hypha growth. Our data suggest that Lip1 activity releases cues from the host surface to promote pathogen development and infection.

The symptoms of tan spot of wheat, caused by Pyrenophora triticirepentis, include a tan necrosis component and an extensive chlorosis component. Since tan spot has become the major component of the leafspotting disease complex of wheat in western Canada, the need for resistant cultivars has increased. This study was conducted to determine whether the resistance to tan spot found in a diverse set of spring and winter wheat genotypes was due to resistance genes not previously reported. The genetic control of resistance to necrosis induced by P. triticirepentis race 1 and race 2 was determined, under controlled environmental conditions, for spring wheat genotypes Erik and 86ISMN 2137 and winter wheat genotypes Hadden, Red Chief, and 6B-365. Plants were inoculated at the two-leaf stage and disease reaction was assessed based on lesion type. Tests of the F(1) and F(2) generations, and of F(2:3) and F(2:8) families, indicated that one recessive gene controlled resistance to the necrosis component of tan spot caused by both race 1 and race 2 in each cross studied. Lack of segregation in crosses between the resistant cultivars indicated that the resistance gene was the same in all of the cultivars.

The genetic control of resistance, expressed as restricted lesion development in seedling plants, to septoria nodorum blotch of wheat was studied under controlled environmental conditions, using the parental, F1, F2, F3, BC1F1, and BC1F2 generations of crosses of Triticum timopheevii-derived resistant durum lines S3-6, S9-10, and S12-1 with the susceptible durum cv. Sceptre. The seedling resistance of these three resistant sources, derived from T. timopheevii (PI 290518), was monogenically controlled. The chromosomal location of the resistance gene identified was determined by crossing the complete set of 'Langdon' - 'Chinese Spring' D-genome disomic substitution lines with S12-1. Tests of the F1 and F2 generations of each cross indicated that only chromosome 3A was associated with resistance. Therefore, the resistance gene is considered to be located on chromosome 3A and has been designated temporarily as SnbTM.

No abstract

Tan spot, a foliar disease of wheat, is caused by the fungus Pyrenophora tritici-repentis. On susceptible wheat cultivars, P. tritici-repentis induces two distinct symptoms: tan necrosis and extensive chlorosis. Presently isolates of P. tritici-repentis are classified into 11 races based on their virulence on a set of wheat differential genotypes. In nature, this pathogen reproduces both sexually and asexually, but the extent of genetic variability in the P. tritici-repentis population of western Canada is unknown. This study was conducted to assess the genetic variability among different isolates of P. tritici-repentis and to determine if similarities among isolates are correlated with race classification or geographic origin of the isolates. Thirty-three isolates of P. tritici-repentis and one isolate each of P. teres f. sp. teres, P. teres f. sp. maculata, P. graminea, Helminthosporium sativum and an uncharacterized isolate were studied with 30 random amplified polymorphic DNA (RAPD) primers. Cluster analysis showed that all isolates had unique banding patterns and that clustering of isolates was independent of their race designation or geographic origin. Analysis of molecular variation (amova) showed that 96.8% of variability occurred among isolates and among race variability accounted for only 3.2% of the total variability. www.blackwell-synergy.com