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Stagonospora nodorum is a foliar pathogen of wheat that produces several host-selective toxins (HSTs) and causes the disease Stagonospora nodorum blotch (SNB). The wheat genes Snn1 and Tsn1 confer sensitivity to the HSTs SnTox1 and SnToxA, respectively. The objectives of this study were to dissect, quantify, and compare the effects of compatible Snn1-SnTox1 and Tsn1-SnToxA interactions on susceptibility in the wheat-S. nodorum pathosystem. Inoculation of a wheat doubled haploid population that segregates for both Snn1 and Tsn1 with an S. nodorum isolate that produces both SnTox1 and SnToxA indicated that both interactions were strongly associated with SNB susceptibility. The Snn1-SnTox1 and Tsn1-SnToxA interactions explained 22 and 28% of the variation in disease, respectively, and together they explained 48% indicating that their effects are largely additive. The Snn1-SnTox1 interaction accounted for 50% of the variation when the population was inoculated with an S. nodorum strain where the SnToxA gene had been mutated, eliminating the Tsn1-SnToxA interaction. These results support the theory that the wheat-S. nodorum pathosystem is largely based on multiple host-toxin interactions that follow an inverse gene-for-gene scenario at the host-toxin interface, but disease exhibits quantitative variation due to the mainly additive nature of compatible interactions. The elimination of either Snn1 or Tsn1 toxin sensitivity alleles resulted in decreased susceptibility, but the elimination of both interactions was required to obtain high levels of resistance. We propose the use of molecular markers to select against Snn1, Tsn1, and other toxin sensitivity alleles to develop wheat varieties with high levels of SNB resistance.

Since the dawn of wheat cytogenetics, chromosome 3B has been known to harbor a gene(s) that, when removed, causes chromosome desynapsis and gametic sterility. The lack of natural genetic diversity for this gene(s) has prevented any attempt to fine map and further characterize it. Here, gamma radiation treatment was used to create artificial diversity for this locus. A total of 696 radiation hybrid lines were genotyped with a custom mini array of 140 DArT markers, selected to evenly span the whole 3B chromosome. The resulting map spanned 2,852 centi Ray with a calculated resolution of 0.384 Mb. Phenotyping for the occurrence of meiotic desynapsis was conducted by measuring the level of gametic sterility as seeds produced per spikelet and pollen viability at booting. Composite interval mapping revealed a single QTL with LOD of 16.2 and r2 of 25.6 % between markers wmc326 and wPt-8983 on the long arm of chromosome 3B. By independent analysis, the location of the QTL was confirmed to be within the deletion bin 3BL7-0.63-1.00 and to correspond to a single gene located ~1.4 Mb away from wPt-8983. The meiotic behavior of lines lacking this gene was characterized cytogenetically to reveal striking similarities with mutants for the dy locus, located on the syntenic chromosome 3 of maize. This represents the first example to date of employing radiation hybrids for QTL analysis. The success achieved by this approach provides an ideal starting point for the final cloning of this interesting gene involved in meiosis of cereals.

Fusarium head blight (FHB), caused mainly by Fusarium graminearum Schwabe, is a destructive disease of wheat (Triticum spp.) in humid growth conditions throughout the world. Genetic resistance of the host plant is considered the most effective and sustainable method of defense against FHB; however, only limited sources of resistance are available in wheat. Relatives of wheat have proven to be an invaluable gene pool for wheat improvement. The objective of this study was to explore relatives of wheat for FHB resistance. We evaluated 293 lines derived from the crosses of wheat with its relatives for resistance to spread of FHB infection over two greenhouse seasons. Of these 293 derivatives, 66 were susceptible, 153 appeared moderately resistant, and 74 lines exhibited a level of resistance comparable with T. aestivum L. 'Sumai 3', the most widely used source of resistance to FHB. Alien species involved in development of these derivatives include T. tauschii (Coss.) Schmal., Roegneria kamoji C. Koch, R. ciliaris (Trin.) Nevski, Leymus racemosus Lam., Thinopyrum ponticum (Podp.) Barkworth & D.R. Dewey, Th. elongatum (Host) D.R. Dewey, Th. junceum (L.) Love, Th. intermedium (Host) Barkworth & D.R. Dewey, Dasypyrum villosa L., Secale cereale L., and oat (Avena sativa L.). The wheat-alien species derivatives identified as resistant to FHB include wheat-alien species amphiploids, synthetic hexaploid wheat lines, and wheat-alien species substitution and translocation lines. These derivatives could serve as novel sources to enhance resistance of wheat to FHB.

Tan spot and Stagonospora nodorum blotch (SNB), caused by fungi Pyrenophora tritici-repentis (Died.) Drechs. [anamorph: Drechslera tritici-repentis (Died.) Shoem.] and Phaeosphaeria nodorum (E. Mller) Hedjaroude [anamorph: Stagonospora nodorum (Berk.) Castellani & Germano], respectively, are two important foliar diseases of wheat (Triticum aestivum L.). The objective of this study was to evaluate the two sets of elite synthetic hexaploid wheat (SHW, 2n = 6x = 42, AABBDD) lines (Elite 1 and Elite 2) developed at the International Maize and Wheat Improvement Center (CIMMYT) for their seedling resistance to P. tritici-repentis and P. nodorum. In this study, 120 elite CIMMYT SHW lines and their durum wheat [T. turgidum subsp. durum (Desf.) Husn.] parents were inoculated with P. tritici-repentis race 1 and a standard field isolate (Sn2000) of P. nodorum, respectively, in two separate three-replication experiments. The seedling reactions to P. tritici-repentis and P. nodorum were evaluated 7 and 10 d postinoculation, respectively. The plant leaves were also infiltrated with the host-selective toxin (HST) Ptr ToxA at the two-leaf stage and sensitivity was evaluated 3 to 4 d postinfiltration. As expected, most SHW lines were the same as their durum parents in their sensitivity to Ptr ToxA because the sensitivity locus Tsn1 is located on chromosome 5B. However, a few of the synthetics were different from their durum parents, suggesting that heterozygosity and heterogeneity might exist in some of the SHW lines and durum parents. The toxin sensitivity significantly increased susceptibility of the synthetics to tan spot but had no significant effects on durum parents. The data showed that 56 (46.7%) and 36 (30.0%) SHW lines were resistant to tan spot and SNB, respectively, whereas resistance was almost absent in the durum parents. These results suggest that the elite CIMMYT synthetics are an excellent source of resistance to tan spot and SNB and should be useful in developing new resistant cultivars and adapted germplasm in bread wheat.

The wheat ( Triticum aestivum L.) stem rust ( Puccinia graminis Pers.:Pers. f.sp. tritici Eriks. and Henn.) resistance gene SrWld1 conditions resistance to all North American stem rust races and is an important gene in hard red spring (HRS) wheat cultivars. A sexually recombined race having virulence to SrWld1 was isolated in the 1980s. Our objective was to determine the genetics of resistance to the race. The recombinant race was tested with the set of stem rust differentials and with a set of 36 HRS and 6 durum cultivars. Chromosomal location studies in cultivars Len, Coteau, and Stoa were completed using aneuploid analysis, molecular markers, and allelism tests. Stem rust differential tests coded the race as TPPKC, indicating it differed from TPMKC by having added virulence on Sr30 as well as SrWld1 . Genes effective against TPPKC were Sr6 , Sr9a , Sr9b , Sr13 , Sr24 , Sr31 , and Sr38 . Genetic studies of resistance to TPPKC indicated that Len, Coteau, and Stoa likely carried Sr9b , that Coteau and Stoa carried Sr6 , and Stoa carried Sr24 . Tests of HRS and durum cultivars indicated that five HRS and one durum cultivar were susceptible to TPPKC. Susceptible HRS cultivars were postulated to have SrWld1 as their major stem rust resistance gene. Divide, the susceptible durum cultivar, was postulated to lack Sr13 . We concluded that although TPPKC does not constitute a threat similar to TTKSK and its variants, some cultivars would be lost from production if TPPKC became established in the field.

'Langdon' (CItr 13165) durum wheat [Triticum turgidum L. subsp. durum (Desf.) Husn., 2n = 4x = 28, AABB] was used as the female and crossed with two accessions oiAegilops tauschii Cosson (2n = 2x = 14, DD), CIae 25 (accession number of USDA National Small Grains Collection, Aberdeen, ID) and RL 5561 (accession number of Cereal Research Centre, Agriculture and Agri-Food Canada, Winnipeg, MB), for SW8 and SW39, respectively. However, some aneuploid plants with chromosome number other than 42 may occur due to unpaired chromosomes in a small number of pollen and egg mother cells as reported in the Largo SHW line (Joppa and Williams, 1982).

Selection of a durum genotype having temperatureinsensitive susceptibility to Pgt-LBBL, indicating that the SrM gene has been eliminated, would increase the utility of PgtLBBL for selection or genetic analysis of new stem rust resistance genes. Rusty will be useful to researchers studying genetics of stem rust resistance in tetraploid wheats or in crosses designed to select monogenic progeny from a parent containing multiple genes for stem rust resistance.

The aneuploid stocks of durum wheat ( Triticum turgidum L. subsp. durum (Desf.) Husnot) and common wheat ( T. aestivum L.) have been developed mainly in 'Langdon' (LDN) and 'Chinese Spring' (CS) cultivars, respectively. The LDN-CS D-genome chromosome disomic substitution (LDN-DS) lines, where a pair of CS D-genome chromosomes substitute for a corresponding homoeologous A- or B-genome chromosome pair of LDN, have been widely used to determine the chromosomal locations of genes in tetraploid wheat. The LDN-DS lines were originally developed by crossing CS nulli-tetrasomics with LDN, followed by 6 backcrosses with LDN. They have subsequently been improved with 5 additional backcrosses with LDN. The objectives of this study were to characterize a set of the 14 most recent LDN-DS lines and to develop chromosome-specific markers, using the newly developed TRAP (target region amplification polymorphism)-marker technique. A total of 307 polymorphic DNA fragments were amplified from LDN and CS, and 302 of them were assigned to individual chromosomes. Most of the markers (95.5%) were present on a single chromosome as chromosome-specific markers, but 4.5% of the markers mapped to 2 or more chromosomes. The number of markers per chromosome varied, from a low of 10 (chromosomes 1A and 6D) to a high of 24 (chromosome 3A). There was an average of 16.6, 16.6, and 15.9 markers per chromosome assigned to the A-, B-, and D-genome chromosomes, respectively, suggesting that TRAP markers were detected at a nearly equal frequency on the 3 genomes. A comparison of the source of the expressed sequence tags (ESTs), used to derive the fixed primers, with the chromosomal location of markers revealed that 15.5% of the TRAP markers were located on the same chromosomes as the ESTs used to generate the fixed primers. A fixed primer designed from an EST mapped on a chromosome or a homoeologous group amplified at least 1 fragment specific to that chromosome or group, suggesting that the fixed primers might generate markers from target regions. TRAP-marker analysis verified the retention of at least 13 pairs of A- or B-genome chromosomes from LDN and 1 pair of D-genome chromosomes from CS in each of the LDN-DS lines. The chromosome-specific markers developed in this study provide an identity for each of the chromosomes, and they will facilitate molecular and genetic characterization of the individual chromosomes, including genetic mapping and gene identification.

The electromagnetic stirring (EMS) effects on peritectic solidification kinetics of undercooled liquid Fe-Ti alloys have been investigated by electrostatic levitation(ESL) and electromagnetic levitation (EML) methods assisted with in-situ diagnostic techniques. The high-sensitivity pyrometer and high-speed camera were employed to monitor the complete solidification process for levitated liquid Fe59Ti41 alloy in undercooling ΔT range of 0 K to 213 K. Theoretical calculations showed that there existed EMS inside electromagnetically levitated alloy melts, and the internal fluid flow dynamics depended on levitation height and melt undercooling. As ΔT rised, the primary dendrite growth velocity V increased according to a power function. Meanwhile, the peritectic recalescence degree ΔTpr and the peritectic recalescence rate Rpr were enhanced gradually, whereas the peritectic recalescence time tpr and the peritectic solidification time tps were shortened linearly. The comparison between ESL and EML experiments revealed that the EMS resulted in four respects of influences including (1) dendrite growth effect, (2) concentration field effect, (3) peritectic reaction effect and (4) microstructure evolution effect. In contrast with ESL, the V of Fe50Ti50 alloy measured by EML was slightly larger at small undercoolings, indicating the EMS affected dendrite growth processes. The solute concentration CL∗ around primary Fe2Ti dendrites for electrostatically levitated liquid Fe59Ti41 alloy deviated far away from original composition, while the EMS homogenized concentration field and the CL∗ variation was weak under EML condition. Both tpr and tps in the absence of EMS were longer that those in the presence of EMS, and it was demonstrated that the EMS accelerated peritectic reaction. Except for microstructure refinement, the EMS modulated the microstructure type and also changed the faceted-growth mode of intermetallic compound phases.