© Australasian Plant Pathology Society 2001 10.1071/AP01021 0815-3191/01/030211 Australasian Plant Pathology, 2001, 30, 211–215 A novel source of resistance in lentil (Lens culinaris ssp. culinaris) to ascochyta blight caused by Ascochyta lentis T. T. Nguyen A , P. W. J. Taylor A , J. B. Brouwer B , E. C. K. Pang C and R. Ford AD A Molecular Plant Genetics and Germplasm Development Group, Department of Crop Production, The University of Melbourne, Victoria 3010, Australia. B Victorian Institute for Dryland Agriculture, Department of Natural Resources and Environment, Private Bag 260, Horsham, Victoria 3401, Australia. C Department of Biotechnology and Environmental Biology, RMIT University, Melbourne, Victoria 3000, Australia. D Corresponding author; email: rebeccaf@unimelb.edu.au Abstract. The lentil accession ILL7537 was resistant in glasshouse bioassays to isolates of Ascochyta lentis Vassilievsky from a range of Australian pathotype groups, confirming its status as a highly resistant cultivated accession. Two dominant complementary genes were determined to condition the genetic mechanism and mode of inheritance of resistance in ILL7537. Accession ILL7537 was screened with molecular markers that were linked to, and flanking, the major resistance gene AbR 1 from the accession ILL5588. The absence of all of the markers from the AbR 1 linkage group indicated that the resistance mechanism in ILL7537 was potentially novel. Introduction Ascochyta blight is caused by Ascochyta lentis Vassilievsky (Kaiser et al. 1997) and is a serious fungal disease of lentil in Australia and worldwide (Kaiser et al. 1997; Nasir 1998). The disease can severely reduce yield (Gossen and Morrall 1983; Brouwer et al. 1995) and quality of the grain (Cromey et al. 1987). The incidence of ascochyta blight can be reduced by treating the seed with a fungicidal dressing (Beauchamp and Morrall 1985; Kaiser and Hannan 1987) or by spraying the crop with foliar fungicides (Beauchamp et al. 1986a; 1986b). Appropriate cultural practices such as using disease-free seed (Morrall and Sheppard 1981), desiccating crops before harvest and harvesting early (Gossen and Morrall 1984), and crop rotation as well as deep ploughing (Gossen and Morrall 1986) also help to reduce the development and spread of the disease. Currently, the most sustainable method of disease control is to use these cultural practices along with resistant genotypes. Isolates of A. lentis are highly variable in their pathogenicity and virulence (Kemal and Morrall 1995; Ahmed et al. 1996; Nasir and Bretag 1997). The host / pathogen interactions for this disease have previously been studied (Kemal and Morrall 1995; Nasir and Bretag 1997; Russell and Hill 1997). In Canada, Kemal and Morrall (1995) concluded that significant differences in disease ratings existed among host differentials and fungal isolates. More recent studies in New Zealand (Russell and Hill 1997) and Australia (Nasir and Bretag 1997; Nasir 1998) have also reported that the interactions between breeding germplasm and isolates from local lentil-growing regions were highly significant or, in other words, isolates of A. lentis were cultivar specific. For the effective exploitation of resistant germplasm, it is important to understand the mechanism of inheritance of the gene(s) controlling the resistance trait. Several mechanisms controlling resistance to A. lentis in lentil have been proposed. Two dominant genes were reported to condition resistance in the accession PI 339283 (Vakulabharanam et al. 1997). One- and two- gene resistance mechanisms were also reported for wild relative genotypes (Ahmad et al. 1997; Ye et al. 2000). A resistance source extensively exploited in the Australian lentil-breeding program was derived from the accession ILL5588. A single major dominant gene (AbR 1 ) conditions foliar resistance in this accession (Ford et al. 1999). Molecular markers have been developed that are closely linked and flank the foliar resistance locus (Ford et al. 1999). These markers are currently being implemented into the Australian breeding programs for marker-assisted selection and incorporation of the resistance into adapted breeding lines. However, more virulent A. lentis pathotypes were able to overcome this resistance (Nasir 1998). This may be due to climatic conditions that are favourable for sexual reproduction, which will enhance genetic mutation and adaptation of the pathogen to the resistant host genotypes. Increased pathogenic variability may also occur through the continued international importation of infected seed. Consequently, other ascochyta blight resistance sources need to be identified and included in current breeding programs. Screening of 22 accessions of lentil in a growth room bioassay with a wide range of Australian and international isolates revealed that accession ILL7537 was the most Resistance to ascochy- ta blight in lentil T. T. Nguyen et al. AP01021