4.7 Article

Molecular-genetic characterisation of a new nematode resistance gene in wheat

Journal

THEORETICAL AND APPLIED GENETICS
Volume 102, Issue 4, Pages 623-629

Publisher

SPRINGER-VERLAG
DOI: 10.1007/s001220051689

Keywords

cereal cyst nematode; resistance genes; wheat introgressions; RFLP; nucleotide binding site-leucine rich repeat Aegilops ventricosa

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Bread wheat lines introgressed with Aegilops ventricosa chromosomes were evaluated for their resistance to the Australian cereal cyst nematode (CCN, Heterodera avenae) pathotype Ha13. Higher levels of resistance relative to the phenotype of the Cre1 CCN resistance gene in wheat were found in the donor Ae. ventricosa parental lines and chromosome-5N(v) substitution or addition lines. The newly identified resistance to pathotype Ha13 on chromosome 5N(v), designated, Cre6, was shown to be independent of the Ae. ventricosa-derived Cre2 gene, effective against several European pathotypes. Another Ae. ventricosa derived gene, Cre5, showed partial resistance to pathotype Ha13. Inhibition of Ha13 female nematode reproduction was ranked in the order Cre6 > Cre1 > CreF greater than or equal to Cre5. Cre6 was inherited as a single dominant locus. Gene sequences encoding nucleotide-binding sites and leucine-rich repeats (NBS-LRR) from the Cre3 CCN-pathotype Ha13 resistance locus were used as probes to isolate related sequences from one of the donor Ae. ventricosa parents. Related sequences from Ae, ventricosa (71-73% similarity at the amino-acid level to the Cre3-derived sequences) of chromosome 5N(v) origin were identified and served as diagnostic molecular markers for the presence of 5N(v). CCN-susceptible plants, found as Variants in some of the purported chromosome 5N(v) lines, were also found to be missing the diagnostic 5N(v) RFLP markers assayed by the NBS-LRR probe. An alloplasmic chromosome-5N(v) addition line with Ae. ventricosa cytoplasm in the wheat cultivar, Moisson, background was particularly variable, with 43% CCN-susceptible plants and a corresponding loss of the diagnostic chromosome-5 molecular markers.

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