No abstract

No abstract

An octoploid triticale was derived from the F| of a Russian wheat aphid-resistant rye, 'Turkey 77', and 'Chinese Spring' wheat. The alloploid was crossed to common wheat, and to 'Imperial' rye/'Chinese Spring' disomic addition lines. ¥, progeny from these ert)sses were tested for Russian wheat aphid resistance and Obanded. A resistance gene(s) was found to be associated with chromosome arm IRS of the 'Turkey 77' rye genome. A monotelosomic IRS ('Turkey 77') addition plant was then crossed with the wheat cultivar 'Gamtoos', which has the IBL.lRS 'Veery' translocation. Unlike the IRS segment in 'Gamtoos', the 'Turkey 77'-derived 1 RS telosome did not express the rust resistance genes SrJI and Lr26, which could then be used as markers. I'rom the F| a mon-oteU^somie IRS addition plant that was also heterozygous for the 1 BL. 1 RS translocation was selected and testcrtissed with an aphtd-susceptible common wheat, 'Inia 66'. Meiotic pairing between the rye arms resulted in the recovery of five euploid Russianwheat-aphid-resistant plants. One recombinant also retained SrJI and Z,r26 and was selfed to produce translocation homozygotes.

Linked leaf rust and stripe rust resistance genes introduced from Triticum dicoccoides protected common wheat seedlings against a range of pathotypes of the respective pathogens. The genes were chromosomally mapped using monosomic and telosomic analyses, C-banding and RFLPs. The data indicated that an introgressed region is located on wheat chromosome arm 6BS. The introgressed region did not pair with the 'Chinese Spring' 6BS arm during meiosis possibly as a result of reduced homology, but appeared to pair with 6BS of W84-17 (57% of pollen mother cells) and 'Avocet S'. The introgressed region had a very strong preferential pollen transmission (0.96-0.98) whereas its transmission through egg cells (0.41-0.66) varied with the genetic background of the heterozygote. Homozygous resistant plants had a normal phenotype, were fertile and produced plump seeds. Symbols Lr53 and Yr35 are proposed to designate the respective genes.

The cultivation of small grain cereals was introduced to South Africa by Dutch settlers in the 17th Century. According to historical records the first documented epidemic of wheat stem rust occurred in the south-western parts of the current Western Cape in 1726. Recurring stem and leaf rust epidemics were associated with expanding wheat production and became particularly severe in the winter-rainfall regions of the Western and Eastern Cape, as well as in the summer-rainfall regions of the Free State. The wheat stripe rust pathogen was first detected in South Africa in 1996. Due to susceptibility of cultivars at the time of this exotic introduction, stripe rust has caused significant losses in commercial wheat production over the past 10 years. Pathotype surveys of Puccinia graminis and P. triticina were initiated in the 1920s, but were discontinued until research on wheat stem rust was resumed in the 1960s. Recent evidence has shown that P. graminis f. sp. tritici continues to evolve. In addition, the annual number of wheat stem rust collections is increasing, emphasising the sustained threat of this damaging pathogen. A stem rust pathotype first detected in 2000, with newly acquired virulence for Sr8b and Sr38, currently constitutes more than 80% of all collections. Leaf and stem rust diseases also occur on barley, oat, triticale, and rye and are important production constraints in several regions. Some studies have described variability in these pathogens but long-term records of pathogenicity changes in barley and oat rust are not available. Cereal rust diseases have clearly played an important role in South African agriculture and many production regions remain favourable for rust development. Current expertise in cereal rusts covers most technologies necessary to study the respective host–pathogen systems. However, a general lack of capacity and fragmentation of research groups prevent a unified approach and remain a challenge for sustainable cereal rust control in South Africa. A national strategy for cereal rust control, with particular emphasis on pathogen and host resources, and breeding for resistance, is urgently needed.

Linked leaf and stripe rust resistance genes introgressed into hexaploid wheat from Aegilops sharonensis provided protection in the seedling stage to a wide range of pathotypes of the two diseases. Monosomic and telosomic analyses showed that the resistance genes occur on wheat chromosome 6A. This result could be confirmed making use of mapped chromosome 6A microsatellite markers. The introgressed chromatin appeared to involve the proximal part of 6AL and the complete 6AS arm and it was thus not possible to deduce the chromosome arm harbouring the resistance genes. The resistance showed non-Mendelian transmission. The genetic background of a heterozygote interacted with the introgressed region to result in either preferential or impaired female transmission. Male transmission appeared to be affected in a different way from female transmission and was exclusive in the genetic background studied. Symbols Lr56 and Yr38 are proposed to designate the respective genes of which line 0352-4 is the appropriate source material.

Chromosome 7D of PI 294994 was indicated as carrying a single dominant gene for resistance to the Russian wheat aphid. The symbol Dn5 is proposed to designate the gene.

The tendency of unpaired meiotic chromosomes to undergo centric misdivision was exploited to translocate leaf rust and stripe rust resistance genes from an Aegilops kotschyi addition chromosome to a group 2 chromosome of wheat. Monosomic and telosomic analyses showed that the translocation occurred to wheat chromosome arm 2DL. The introgressed region did not pair with the corresponding wheat 2DL telosome during meiosis suggesting that a whole arm may have been transferred. Female transmission of the resistance was about 55% whereas male transmission was strongly preferential (96%). The symbols Lr54 and Yr37 are proposed to designate the new resistance genes.