Abstract:

The increasing evolution and aggressiveness of wheat rust pathogens with high virulence against widely deployed resistance genes constitutes a major threat to the global wheat production and consequently food security. The changes in the pathogenicity and environmental adaptation of these fungi have resulted in serious epidemics and in some cases total crop loss. In order to develop appropriate rust control measures, there is a need to understand the current pathogen-environment interactions; mechanisms of pathotype evolution, and pathogenic (virulence/avirulence) dynamics against the existing resistance genes. Host resistance is the major and most economically viable rust control strategy, having the capacity to significantly reduce wheat yield loss and fungicide use if effectively utilised. The challenge posed by changing rust pathogens calls for the application of advanced techniques, so that efforts to breed for durable resistance can be sped up. However, the need to expand the wheat rust resistance gene pool is crucial today. Therefore, the aims of this research were to study and understand the basis of genetic variability among selected Australian pathotypes of Puccinia graminis f. sp. tritici (Pgt) and to identify new sources of leaf rust, stem rust and stripe rust resistance in two wheat germplasm collections, one from Africa and one comprising mainly spring wheat landraces. These studies examined genetic variability among 157 Pgt isolates collected over a 39 year period in Australia, that were chosen to represent two putative closely related clonal lineages derived from two founding pathotypes (pts.) 326-1,2,3,5,6 (founder of Lineage 3), and 194- 1,2,3,5,6 (founder of Lineage 4). Representative isolates from Lineages 1 (pt. 126-5,6,7,11), 2 (pt. 21-0), and Lineage 5 (pts. 34-2,4,5,6,7,11 and 34-2,3,5,7), were also included as controls. Pathogenicity tests of all purified isolates on standard differential genotypes showed general consistency in avirulence and virulence patterns with previous research reports implying that they were actual representatives of the original pathogen cultures. Via cluster analysis, the 99 isolates representing Lineage 3 and Lineage 4 grouped together, indicating similarity in their pathogenicity against the known resistance genes. The level of variation in pathogenicity observed among the subgroups of the 99 isolates resulted from the pathotypes with uncommon or additional virulence. Because single-step mutation is believed to be the major mechanism via which most of these pathotypes have evolved in Australia, it was expected that pathotypes within Lineages 3 and 4 should show very little genetic diversity. Assessments with six SSR markers clearly showed the genetic similarity of isolates within Lineages 2, 3 and 4, and their distinctiveness from isolates from Lineage 1, consistent with the independent origins of eachfounding isolate. A further analysis of Lineage 3 and Lineage 4 using seven SSR markers with higher polymorphism revealed some level of genetic diversity among the pathotypes. The 34 SSR genotypes detected among the 142 isolates were characterised by very low genetic variation (F$r= 0.042), which implied that these pathotypes were genetically related, further confirming that they were clonal thus evolving from each other via mutation. However, the existing genetic variations among the genotypes originate from the different forms and rates of mutation which vary per locus.