Four newly detected accessions of wild barley (Hordeum vulgare ssp. spontaneum) resistant to powdery mildew caused by Blumeria graminis f. sp. hordei were studied with the aim of finding the number of genes/loci conferring the resistance of individual accessions, the type of inheritance of the genes and their relationships to the Mla locus. F 2 populations after crosses between the winter variety 'Tiffany' and four wild barley accessions and use of microsatellite DNA markers were focused on the identification of individual resistance genes/loci by means of their chromosomal locations. In PI466495, one locus conferring powdery mildew resistance was identified in highly significant linkage with the marker Bmac0213. This location is consistent with the known locus Mla on chromosome 1HS. In the other three accessions the resistance was determined by two independent loci. In PI466197, PI466297 and PI466461, one locus was identified on chromosome 1HS and three new loci were revealed on chromosomes 2HS (highly significant linkage with Bmac0134), 7HS (highly significant linkage with Bmag0021) and 7HL (significant linkage with EBmac0755). Our prospective aim is identification of further linked DNA markers and the exact location of the resistance genes on the barley chromosomes.

We studied the effect of three factors on the induction of (FT) after 5-azaC treatment was observed. On the contrary, flowering in Arabidopsis thaliana, i.e. vernalization, day only five mutants -dl, pm, M63, M73 and fca-1 -showed a length and DNA demethylation. Seven natural late flowering shortening of the FT, while in the majority of the late genotypes and 13 late flowering mutants were used in the flowering mutants, no significant response (earlier flowering) was found. The different response to the vernalization and experiments. The effect of the vernalization and the short day (SD) was uniform in all genotypes used, resulting in shorten-demethylation treatment in late flowering mutants shows the ing (vernalization) or extension of the period before the possibility of two different pathways leading to the flowering, appearance of the first flower primordia. On the other hand, both of which are regulated by DNA demethylation. The the effect of the demethylating agent (5-azacytidine [5-azaC]) different response of natural and induced late flowering genotypes after 5-azaC treatment shows that genes that play a role was not uniform in the genotypes used. In all natural late in flower development are of a different nature. genotypes (except Lu-1), the shortening of the flowering time

In PI466495, a powdery mildew resistance source of wild barley (Hordeum vulgare ssp. spontaneum), one gene conferring powdery mildew resistance was identified in the Mla locus. In this paper, the RGH1a gene sequence was used as source for the development of a cleaved amplified polymorphic sequence (CAPS) marker. Co-segregation between this marker and powdery mildew resistance was analysed by specific DNA fragments associated with each allele of the gene using 286 F 2 plants derived from a cross between winter barley (H. vulgare L.) variety 'Tiffany' and PI466495. For the co-dominant marker RGH1aI1a, three fragments, 370 bp, 82 bp and 59 bp in size, were amplified from F 2 plants exhibiting resistance reaction types 0 and 0-1 to powdery mildew; whereas two fragments, 429 bp and 82 bp in size, were amplified in susceptible plants. Simple procedures based on polymerase chain reaction and restriction enzyme digestion allowed for identifying the plants susceptible to powdery mildew (Blumeria graminis f. sp. hordei) and plants homozygous or heterozygous for the resistance allele. The RGH1aI1a marker was positioned 0.85 cM to the resistance gene and the efficiency of marker-assisted selection (MAS), evaluated as the probability of crossing-over between the marker and the targeted gene, was 99%. The CAPS marker RGH1aI1a is a valuable candidate for MAS and gene transfer into barley varieties susceptible to powdery mildew.

The accession PI466197 of wild barley (Hordeum vulgare ssp. spontaneum) with a newly identified resistance to powdery mildew caused by Blumeria graminis f.sp. hordei was studied with the aim to localise the genes determining resistance on a barley genetic map using DNA markers. Molecular analysis was performed in the F2 population of the cross between the winter variety ‘Tiffany’ and the resistant accession PI466197, consisting of 113 plants. DNA markers, 17 simple sequence repeats (SSRs), four sequence‐tagged sites (STSs) and one cleaved amplified polymorphic sequence (CAPS) marker developed from the Mla locus sequence were used for genetic mapping and a two‐locus model of resistance was shown. One of the resistance genes originating from H. vulgare ssp. spontaneum PI466197 was localised between the markers RGH1aE1 and Bmac0213 on the short arm of chromosome 1H, which is the position consistent with the Mla locus. The other gene was proven to be highly significantly linked with GBMS247, Bmac0134 and MWG878 on the short arm of chromosome 2H. The flanking markers were Bmac0134 and MWG878, assigned 4 and 8 cM from the resistance gene, respectively. Until now, no gene conferring powdery mildew resistance originating from H. vulgare has been located on the short arm of barley chromosome 2H.

Thirteen accessions of wild barley (Hordeum vulgare ssp. spontaneum) resistant to powdery mildew caused by the fungus Blumeria graminis f. sp. hordei were studied with the aim of determining the number of resistance genes and their allelic relationships to the Mla locus on the short arm of chromosome 1H. In five accessions (PI391130, PI466193, PI466200, PI466495 and PI466510), the resistance was caused by one gene, in seven accessions (PI354949, PI391081, PI466158, PI466197, PI466211, PI466297 and PI466461) by two independent genes and in PI301004 by three independent genes. The type of inheritance of all analysed genes except two was dominant or semi-dominant; only one of two genes in PI391081 and PI466297 was recessive. Allelism tests confirmed that in 10 accessions one gene was allelic with the Mla locus, and in three accessions (PI391081, PI466193 and PI466297) the resistance genes were different from the Mla locus.