More than 50 leaf rust resistance (Lr) genes against the fungal pathogen Puccinia triticina have been identified in the wheat gene pool, and a large number of them have been extensively used in breeding. Of the 50 Lr genes, all are known only from their phenotype and͞or map position except for Lr21, which was cloned recently. For many years, the problems of molecular work in the large (1.6 ؋ 10 10 bp), highly repetitive (80%), and hexaploid bread wheat (Triticum aestivum L.) genome have hampered map-based cloning. Here, we report the isolation of the Lr gene Lr10 from hexaploid wheat by using a combination of subgenome map-based cloning and haplotype studies in the genus Triticum. Lr10 is a single-copy gene on chromosome 1AS. It encodes a CC-NBS-LRR type of protein with an N-terminal domain, which is under diversifying selection. When overexpressed in transgenic wheat plants, Lr10 confers enhanced resistance to leaf rust. Lr10 has similarities to RPM1 in Arabidopsis thaliana and to resistance gene analogs in rice and barley, but is not closely related to other wheat Lr genes based on Southern analysis. We conclude that map-based cloning of genes of agronomic importance in hexaploid wheat is now feasible, opening perspectives for molecular bread wheat improvement trough transgenic strategies and diagnostic allele detection.

A recessive mutation of Arabidopsis designated sas1 (for sodium overaccumulation in shoot) that was mapped to the bottom of chromosome III resulted in a two-to sevenfold overaccumulation of Na ؉ in shoots compared with wild-type plants. sas1 is a pleiotropic mutation that also caused severe growth reduction. The impact of NaCl stress on growth was similar for sas1 and wild-type plants; however, with regard to survival, sas1 plants displayed increased sensitivity to NaCl and LiCl treatments compared with wild-type plants. sas1 mutants overaccumulated Na ؉ and its toxic structural analog Li ؉ , but not K ؉ , Mg 2 ؉ , or Ca 2 ؉ . Sodium accumulated preferentially over K ؉ in a similar manner for sas1 and wild-type plants. Sodium overaccumulation occurred in all of the aerial organs of intact sas1 plants but not in roots. Sodium-treated leaf fragments or calli displayed similar Na ؉ accumulation levels for sas1 and wild-type tissues. This suggested that the sas1 mutation impaired Na ؉ long-distance transport from roots to shoots. The transpiration stream was similar in sas1 and wild-type plants, whereas the Na ؉ concentration in the xylem sap of sas1 plants was 5.5-fold higher than that of wild-type plants. These results suggest that the sas1 mutation disrupts control of the radial transport of Na ؉ from the soil solution to the xylem vessels. INTRODUCTIONAmong abiotic stresses, salinity is one of the major causes of yield losses of crop plants (Boyer, 1982). Salt stress is a polymorphous stress that reduces yield through three direct effects: osmotic stress, nutritional stress, and ion toxicity. It is widely thought that breeding for salt tolerance will involve developing a pyramiding strategy for selecting favorable combinations of traits, each of which would improve one of the physiological adaptations to salt stress (Yeo and Flowers, 1986). However, it is not clear which traits are appropriate for use in breeding programs to improve salt tolerance. Many physiological and molecular responses to salinity have been described (Greenway and Munns, 1980;Munns, 1993;Yeo, 1998), but their effects on the improvement of salt tolerance have seldom been demonstrated. This observation made clear the necessity of developing genetic approaches to establish which responses are physiologically relevant to salt tolerance (Epstein et al., 1980).The contributions of different physiological responses to salt tolerance were analyzed recently in genetic studies with a number of different variants (mutants or transgenic plants). The advantages of using mutants are that no prior knowledge of the molecular bases of the mechanism of interest is necessary and that mutants can reveal mechanisms previously unknown to be involved in salt tolerance. The identification and characterization of salt-tolerant and salt-hypersensitive mutants have drawn attention to several matters: (1) the control of Cl Ϫ transport from root to shoot (Abel, 1969); (2) the overaccumulation of proline (Kueh and Bright, 1982); (3) the overaccumulation of Na ϩ and K ϩ ...