Molecular Characterization of Australian Isolates of Puccinia graminis f. sp.  tritici Supports Long-Term Clonality but also Reveals Cryptic Genetic Variation. 
Long-term surveys of pathogenicity in Puccinia graminis f. sp.  tritici in Australia have implicated mutation as a major source of virulence, at times leading to the demise of stem-rust-resistant wheat cultivars and substantial yield losses.  Since 1925, these surveys have identified at least four occasions on which exotic isolates of P. graminis f. sp.  tritici appeared in Australia, with each acting as a founding isolate that gave rise sequentially to derivative pathotypes via presumed single-step mutation.  The current study examined the relationship between virulence and molecular patterns using simple-sequence repeat (SSR) markers on selected isolates of P. graminis f. sp.  tritici collected in Australia during a 52-year period in order to propose an evolutionary pathway involving these isolates.  Studies of SSR variability among this collection of isolates within a putative clonal lineage based on pathotype 21-0, first detected in 1954 (the "21/34 lineage"), provided compelling evidence of clonality over the 52-year period, coupled with single-step acquisition of virulence for resistance genes.  It also supported the postulation that two triticale-attacking pathotypes (34-2,12 and 34-2,12,13) detected in the early 1980s were derived from pathotype 21-0 via stepwise sequential acquisition of virulence for Sr5, Sr11, Sr27, and then SrSatu.  Some of the isolates examined that were regarded as members of the race 21/34 lineage based on pathogenicity differed significantly in their SSR genotypes, indicating that they may have originated from processes more complex than simple mutation.  This included two isolates of pathotype 21-0, which were collected in 1994 and 2006.  Given that sexual recombination in P. graminis is rare or absent in Australia, the cryptic complexity observed could indicate that one or more of these isolates arose as a consequence of asexual recombination.