NORTH DAKOTA
USDA-ARS CEREAL CROPS RESEARCH UNIT
Northern Crop Science Laboratory, North Dakota State University, Fargo, ND 58078, USA.
Justin D. Faris, Sunil Kumar, and Timothy L. Friesen.
Fusarium head blight caused by F.
graminearum is one of the most destructive diseases of durum and common wheat.
Promising sources of FHB resistance have been identified among common (hexaploid) wheats, but the same is not
true for durum (tetraploid) wheats. Triticum turgidum subsp. dicoccoides, or wild emmer wheat, is a potential
tetraploid source of FHB resistance. A previous study indicated that chromosome 7A from T. turgidum subsp. dicoccoides accession PI478742 contributed significant levels of resistance to FHB. In this study, a genetic linkage map of
chromosome 7A was constructed in a population of 118 recombinant inbred lines derived from a cross between the durum
cultivar Langdon (LDN) and a disomic LDNT. turgidum subsp. dicoccoides PI478742 chromosome 7A substitution line
[LDNDIC 7A(742)]. The population was evaluated for type-II FHB resistance in three greenhouse seasons. Interval
regression analysis indicated that a single QTL designated Qfhs.fcu-7AL explained 19% of the phenotypic variation and spanned
an interval of 39.6 cM. Comparisons between the genetic map and a previously constructed physical map of
chromosome 7A indicated that Qfhs.fcu-7AL is located in the proximal region of the long arm. Combine Qfhs.fcu-7AL with the QTL Qfhs.ndsu-3AS in order to develop durum wheat germ plasm and cultivars with higher levels of FHB resistance would
be beneficial.
Timothy L. Friesen, Justin D. Faris, and Richard Oliver.
We have recently shown that St. nodorum produces multiple proteinaceous host selective toxins. These toxins
include SnToxA, a host selective toxin first isolated from P. tritici-repentis, which has been implicated in a very recent
horizontal gene transfer event from St.
nodorum to P. tritici-repentis. Strong evidence has implicated SnToxA, as well as
SnTox1, SnTox2, and SnTox3 as significant factors in SNB disease. Each toxin has been shown to interact either directly
or indirectly with single dominant host sensitivity genes designated as Tsn1 (SnToxA), Snn1 (SnTox1), Snn2 (SnTox2), and Snn3 (SnTox3). Using mapping populations segregating for multiple toxin sensitivities, disease significance for
each toxin sensitivity gene has been shown to account for as much as 60% of the disease caused by St. nodorum isolates producing each toxin. Other than SnToxA and SnTox1, 2, and 3, at least three additional host selective toxins and
their host sensitivity genes have been identified and disease significance data is being collected. This work shows that the S. nodorum pathosystem is a model inverse-gene-for-gene system where at least seven proteinaceous host selective
toxins produced by the pathogen interact directly or indirectly with dominant sensitivity/susceptibility genes in the host to
cause disease.
Leela Reddy, Timothy L. Friesen, Steven W. Meinhardt, Shiaoman Chao, and Justin D. Faris.
SnTox1 is a host-selective proteinaceous toxin produced by the wheat pathogen St. nodorum, and it is known to play a major role in causing disease. Sensitivity to SnTox1 is governed by a single dominant gene designated Snn1, which maps within a major gene rich region on the short arm of chromosome 1B. We conducted saturation mapping of the Snn1 region using SSRs, RFLPs, and over 50 ESTs that map within deletion bin 1BSsat18-0.50-1.00. Flanking markers were used to initiate fine-mapping in a population of more than 8,000 gametes. The Langdon durum BAC library was used to construct a physical contig spanning about 500 kb at the Snn1 locus. Comparisons between the physical and genetic distances indicate that recombination frequencies are highly variable within the region harboring Snn1. Sequencing and annotation of the BAC contig revealed that genes are not randomly distributed, but a number of the predicted genes are strong candidates for Snn1. The isolation of Snn1 will allow us to begin the characterization of the interactions associated with the wheatSt. nodorum pathosystem.
Huangjun Lu, John P. Fellers, Steven W. Meinhardt, Timothy L. Friesen, and Justin D. Faris.
The wheat Tsn1 gene confers sensitivity to the host-selective proteinaceous toxins Ptr ToxA and SnToxA produced by
the pathogenic fungi P. tritici-repentis and St. nodorum, respectively. A positional cloning strategy is being used to
clone this gene. An F2 population consisting of 5,438 gametes was developed for high-resolution mapping. Multiple
chromosome walking steps in conjunction with complete sequencing of BACs identified in the Langdon durum BAC
library were performed. A total of 14 BACs were sequenced and assembled into two contigs that together spanned more than
1 Mb. Mapping results indicated that one contig spanned the Tsn1 gene. The Tsn1 candidate region is about 300 kb in
size and contains nine putative genes. Four of the putative genes have been disproved to be Tsn1 by comparative sequence analysis of Langdon EMS-induced Tsn1-disrupted mutants with the wild type. We are continuing the systematic
testing of the remaining candidates to determine which candidate is Tsn1. The isolation of Tsn1 will allow us to begin
deciphering the molecular interactions and mechanisms associated with the
wheatP. tritici-repentis and
wheatSt. nodorum pathosystems.
Zengcui Zhang, Kristin J. Simons, and Justin D. Faris.
The Q gene of wheat is responsible for many morphological traits associated with domestication. Q is located on wheat chromosome 5A and it is a member of the AP2 class of transcription factors. Genotypes harboring the q allele on chromosome 5A have speltoid spikes, which include non free-threshing seed, tough glumes, and other primitive characteristics. Homoeoalleles of Q exist on chromosomes 5B and 5D, but their functions are unknown. Here, we initiated the structural and functional characterization of the 5D homoeoallele of the Q gene (5Dq). Evaluation of deletion mutants indicated that 5Dq also contributes to the suppression of speltoid characters, but to a lesser degree than does the Q allele on 5A. The genomic sequence of 5Dq is 3,254 bp and is alternately spliced producing two transcriptional variants in spike tissue. One variant resulted from the splicing of ten exons that corresponded to the splicing structure of 5AQ/q alleles, and encodes a predicted protein of 452 amino acids. The other variant lacked the splicing of the first intron, which resulted in a frameshift that led to a stop codon within the first AP2 domain. Sequence alignments of 5AQ and 5Dq indicated that they shared 90 and 94% identity at the nucleic acid and amino acid levels, respectively. RTPCR experiments indicated that 5Dq is expressed in immature spikes. Characterization of the q homoeoalleles will provide insights regarding polyploid gene regulation of genetic networks associated with domestication and morphology.
Chenggen Chu, Justin D. Faris, Timothy L. Friesen, Steven S. Xu.
Hybrid necrosis is the gradual premature death of leaves or plants in certain F1 hybrids of wheat, and it is caused by the interaction of two dominant complementary genes Ne1 and Ne2 located on chromosome arms 5BL and 2BS, respectively. To date, molecular markers linked to these genes have not been identified and linkage relationships of the two genes with other important genes in wheat have not been established. We observed that the F1 hybrids from the crosses between the bread wheat cultivar Alsen and four synthetic hexaploid wheat (SHW) lines (TA4152-19, TA4152-37, TA4152-44, and TA4152-60) developed at CIMMYT exhibited hybrid necrosis. This study was conducted to determine the genotypes of TA4152-60 and Alsen at the Ne1 and Ne2 loci and to map the genes using microsatellite markers in backcross populations. Genetic analysis indicated that Alsen has the genotype ne1ne1Ne2Ne2, whereas the SHW lines have Ne1Ne1ne2ne2. The microsatellite marker Xbarc74 was linked to Ne1 at a genetic distance of 2.0 cM on chromosome arm 5BL, and Xbarc55 was 3.2 cM from Ne2 on 2BS. Comparison of the genetic maps with the chromosome deletion-based physical maps indicated that Ne1 lies in the proximal half of 5BL, whereas Ne2 is in the distal half of 2BS. Genetic linkage analysis showed that Ne1 was about 35 cM proximal to Tsn1, a locus conferring sensitivity to the host selective toxin Ptr ToxA produced by the tan spot fungus. The closely linked microsatellite markers identified in this study can be used to genotype parental lines for Ne1 and Ne2 or to eliminate the two hybrid necrosis genes using marker-assisted selection.
Jing Li, Daryl L. Klindworth, Xiwen Cai, Jinguo Hu, and Steven S. Xu.
The aneuploid stocks of durum wheat and common wheat have been developed mainly in the cultivars Langdon
(LDN) and Chinese Spring (CS), respectively. The LDNCS 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 for determining chromosomal locations of genes in tetraploid wheat. The LDN
DS lines were originally developed by crossing CS nulli-tetrasomics to LDN followed by six backcrosses with LDN.
They have subsequently been improved by five additional backcrosses with LDN. The objectives of this study were
to characterize a set of the most recent 14 LDN DS lines and 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 two 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 three genomes. A comparison of the source of the 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 one fragment specific to that chromosome or group, suggesting that the
fixed primers might generate markers from target regions. The TRAP marker analysis verified the retention of at least 13
pairs of A- or B-genome chromosomes from LDN and one 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.
Daryl L. Klindworth, James D. Miller, Yue Jin, and Steven S. Xu.
The genetics of resistance to stem rust in durum wheat is not as well understood as for bread wheat. Our objective was to determine the chromosomal location of genes for stem rust resistance in four monogenic lines derived from the Ethiopian tetraploid landrace ST464. The four monogenic lines were crossed to a set of stem rust susceptible aneuploids based on the tetraploid line 47-1. We observed chromosome pairing in the hybrids and made testcrosses to Rusty durum. Monogenic lines ST464-A1 and ST464-A2 were observed to carry a 2A/4B translocation, and subsequent crosses proved that the translocation was derived from ST464. Testcross F2 seedlings were inoculated with one of three stem rust pathotypes and classified for segregation for resistance to identify the critical chromosome for each monogenic line. The stem rust resistance genes in monogenic lines ST464-A1, ST464-A2, and ST464-C1 were located to chromosomes 6A, 2B, and 6A, respectively. The gene in ST464-B1 may be located to chromosome 4A, as it appeared it was not located on any of the other 13 chromosomes. The four ST464 monogenic lines and hexaploid lines carrying Sr9e and Sr13 were then tested with eight stem rust pathotypes with the objective of postulating the genes present in the monogenic lines. The genes in ST464-A2 and ST464-C1 were postulated to be Sr9e, and Sr13, respectively.
Shiaoman Chao, Wenjun Zhang, Jorge Dubcovsky, and Mark Sorrells.
Genetic diversity and genome-wide linkage disequilibrium (LD) were investigated among 43 U.S. wheat elite
cultivars and breeding lines representing seven U.S. wheat market classes using 242 wheat genomic SSR markers
distributed throughout the wheat genome. These lines were selected from 18 wheat breeding programs across the U.S. as part of
a collaborative Wheat Coordinated Agricultural Project funded by USDACSREES (http://maswheat.ucdavis.edu/).
Genetic diversity among these lines was examined using genetic distance-based and model-based clustering
methods, and analysis of molecular variance. Four populations were identified from the model-based analysis, which
partitioned each of the spring and winter populations into two subpopulations, corresponding largely to major geographic regions
of wheat production in the US. This suggests that the genetic diversity existing among this U.S. wheat germ plasm
was influenced more by regional adaptation than by market class, and the individuals clustered in the same
model-based population shared related ancestral lines in their breeding history. For this germ plasm collection, genome-wide
LD estimates were generally less than 1 cM for genetically linked loci pairs. This may result from the population
stratification and small sample size that reduced statistical power. Most of the LD regions observed were between loci less
than 10 cM apart. However, the distribution of LD was not uniform based on linkage distance and was independent of
marker density. Consequently, LD is likely to vary widely among wheat populations and caution must be used in
designing association studies in wheat.
For inquiries and requests:
Summary of stocks maintained:
Langdon durumT. turgidum subsp. dicoccoides disomic substitution lines. Three sets of Langdon durumT. turgidum subsp. dicoccoides (LDN-DIC) substitution lines were developed by Dr. Leonard R. Joppa using T. turgidum subsp. dicoccoides (DIC) accessions Israel-A, PI-481521 and PI-478742 as the chromosome donor in Langdon background (Table 1). In these lines, a pair of chromosomes from DIC was substituted for a pair of native homologous chromosomes in LDN. The LDN-DIC lines were produced by crossing each Langdon durum D-genome disomic substitution line (LDN D-genome DS) as female to each of three DIC accessions. Five to seven backcrosses were made to the LDN D-genome DS to restore the LDN genetic background, while retaining a single chromosome from DIC as a monosome. The LDNDIC lines were selected after one generation of self-pollination of BC5 to BC7 plants. The sets based on PI-481521 and Israel-A have all 14 chromosome substitutions. But, three substitutions (2A, 3A, and 3B) in the set based on PI-478742 are not available.
| Israel-A | PI481521 | PI478742 | |
|---|---|---|---|
| 1A | LDNDIC 1A(IsA) |
LDNDIC 1A(521) |
LDNDIC 1A(742) |
| 2A | LDNDIC 2A(IsA) |
LDNDIC 2A(521) |
|
| 3A | LDNDIC 3A(IsA) |
LDNDIC 3A(521) |
|
| 4A | LDNDIC 4A(IsA) |
LDNDIC 4A(521) |
LDNDIC 4A(742) |
| 5A | LDNDIC 5A(IsA) |
LDNDIC 5A(521) |
LDNDIC 5A(742) |
| 6A | LDNDIC 6A(IsA) |
LDNDIC 6A(521) |
LDNDIC 6A(742) |
| 7A | LDNDIC 7A(IsA) |
LDNDIC 7A(521) |
LDNDIC 7A(742) |
| 1B | LDNDIC 1B(IsA) |
LDNDIC 1B(521) |
LDNDIC 1B(742) |
| 2B | LDNDIC 2B(IsA) |
LDNDIC 2B(521) |
LDNDIC 2B(742) |
| 3B | LDNDIC 3B(IsA) |
LDNDIC 3B(521) |
|
| 4B | LDNDIC 4B(IsA) |
LDNDIC 4B(521) |
LDNDIC 4B(742) |
| 5B | LDNDIC 5B(IsA) |
LDNDIC 5B(521) |
LDNDIC 5B(742) |
| 6B | LDNDIC 6B(IsA) |
LDNDIC 6B(521) |
LDNDIC 6B(742) |
| 7B | LDNDIC 7B(IsA) |
LDNDIC 7B(521) |
LDNDIC 7B(742) |
LDNDIC recombinant-inbred, chromosome-substitution lines (RICLs). Homozygous recombinant populations were developed by crossing each of the available LDNDIC (Israel A accession) substitution lines with LDN as described in Joppa (1997; Crop Science 33:908-913). Maps have been generated for some of the populations (see Table 2). In addition, RIL populations have been developed for the LDNDIC 5B (PI478742) and LDNDIC 7A (PI478742) lines.
89Population |
No. lines |
|---|---|
LDNDIC 1A(IsA) HR |
92 |
LDNDIC 1B(IsA) HR |
93 |
LDNDIC 2A(IsA) HR |
107 |
LDNDIC 3A(IsA) HR |
83 |
LDNDIC 3B(IsA) HR |
91 |
LDNDIC 4A(IsA) HR |
136 |
LDNDIC 4B(IsA) HR |
117 |
LDNDIC 5A(IsA) HR |
95 |
LDNDIC 5B(IsA) HR |
136 |
| LDNDIC 6A(IsA) HR | 89 |
| LDNDIC 6B(IsA) HR | 85 |
| LDNDIC 7A(IsA) HR | 166 |
| LDNDIC 7B(IsA) HR | 148 |
| LDNDIC 5B(742) RI | 125 |
| LDNDIC 7A(742) RI | 125 |
Langdon D-genome substitution lines. The Langdon D-genome substitutions were developed by crossing the Chinese Spring nullisomic-tetrasomic series to Langdon durum wheat. The Chinese Spring aneuploids have four copies of a chromosome and have no copies of a homoeologous chromosome. Thus, CS N1A/T1D can be crossed to Langdon durum, a tetraploid that does not have the D-genome chromosomes. The F1 from this cross has 14 pairs of chromosomes, including a pair of 1D chromosomes and also has seven univalent chromosomes including a monosome for 1A. Selfing and selecting will result in plants with 14 pairs of chromosomes and no monosomics. These plants will be disomic for 1D and nullisomic for 1A. All possible combinations of plants with the disomic D-genome chromosomes and nullisomic for the A- and B-genome homoeologues were obtained.
In order to eliminate the genes contributed to the A and B genomes by the CS parent, the plants were backcrossed to Langdon 12 times. We hope that almost all contribution to these lines from CS has been eliminated except for the contribution of the homozygous D-genome chromosomes.
In some cases, the D-genome chromosomes fail to completely compensate for the loss of the homoeologous A- or B-genome chromosomes. A description of these lines follows. If a line is not mentioned, it should be assumed that it is normal.
LDN-4D(4A). The plants nullisomic for chromosome 4A do not germinate and no plants of this constitution have ever been observed. The line is maintained as 13" + 1"4D + 1'4A. Selfing these plants results in plants like the parent except for occasional plants with 15" (4D disomic additions). These plants should always be used as the female in crosses and the progeny will almost always be 13" + 2' (i.e., M4A, M4D).
LDN-5D(5A). Plants nullisomic for chromosome 5A have very low fertility. Consequently, this line is maintained as disomic for 5D and monosomic for 5A. The 14" + 1' plants produce progeny like the parent (i.e. 14" + 1'). There are occasional 15" plants. We usually discard these plants using root tip analysis of seedlings.
LDN-3D(3B). Sears reported that chromosome 3B contains a gene that is necessary to prevent asynapsis at MI of meiosis. The 3D(3B) line must have the short arm of 3B and we maintain the line as the disomic 3D, monosomic 3B. Transmission of the 3B chromosome is low. Thus, it is necessary to look at root tips to find plants with the 3B monosome. Plants that are disomic for both 3D and 3B are possible to obtain, but they are abnormal and very hard to maintain. We continue to search for better plants and for plants with a telosomic 3B chromosome.
LDN-5D(5B). The Ph1 gene is on the long arm of chromosome 5B. When this gene is absent, pairing between non-homologous chromosomes is observed. Selfing plants nullisomic for chromosome 5B results in the line running out after a few generations; due to translocations, duplications, and deficiencies. The line is maintained as disomic for 5D and monosomic for 5B. Transmission of the monosomic 5B chromosome averages about 50 percent in selfed plants.
LDN-6D(6B). Plants nullisomic for 6B and disomic for 6D have very low fertility. Examination of the heads reveals that many of the anthers resemble pistils (i.e., plants are pistilloid). We maintain this line with a telosomic 6BS chromosome. Transmission of the 6BS telosome through the male gamete is close to 100 percent. Occasional plants disomic for 6BS are observed. Because of the male transmission of this telo, crosses should be made with the 6D(6B) line as the female. The telo is seldom transmitted through female gametes.
LDN-7D(7B). The group-7 chromosomes have genes governing chlorophyll production. Chromosome 7D does not completely compensate for either 7A or 7B, but the problem is greater in the case of 7B. The plants tend to be somewhat weak. At heading, the leaves develop a progressive necrosis that eventually leads to plant death, but this does not occur before the plants set seed. Pollen for crossing is sometimes difficult to obtain. Seed production is adequate for most purposes.
Langdon durum-Ae. tauschii synthetic hexaploid wheat. Dr. Joppa developed a number of spontaneous synthetic hexaploid wheat from partially fertile hybrids between LDN and different Ae. tauschii accessions in 1980s. We recently developed three new synthetic lines from the crosses between LDN and Ae. tauschii accessions PI 476874 (tough rachis), CIae19, and AL8/78. Some Ae. tauschii accessions were received from National Small Grains Collection (NSGC), Aberdeen, ID, others were provided respectively by Dr. E.R. Kerber (Agriculture and Agri-Food Canada, Winnipeg, Manitoba, Canada), Dr. E. Nevo (University of Haifa, Haifa, Israel), and Dr. B. Keller (University of Zurich, Zurich, Switherland). Except that the synthetic line from cross LDN/PI 268210 was named as Largo and released as greenbug-resistant germplasm, other lines have not been characterized previously. These synthetics have recently been evaluated for resistance to tan spot, Stagonospora leaf blotch, leaf and stem rust, and Hessian fly. We currently are evaluating their resistance to FHB and seed storage protein compositions. The synthetics that are available for seed distribution are listed in Table 3.
Durum wheat T1AS·1AL-1DL translocation lines carrying Glu-D1d. Four translocation lines having the pedigree Langdon1D(1A)/Len//Langdon/3/2*Renville and carrying glutenin subunits 1Dx5 and 1Dy10 from the Glu-D1d allele are available. These lines were produced in an effort to develop dual-purpose (good baking and pasta quality) durum wheat. The lines are identified as L092, L252, S99B33, and S99B34. Three of the lines carry the LMWII banding pattern derived from Renville and conditioned by the Glu-B3 gene. The fourth line, L252, carries the LMWI banding pattern derived from Langdon. Quality tests have indicated L252 has better mixing traits and slightly better loaf volume than the translocation lines carrying LMWII. In trials conducted in North Dakota from 2000-2002, S99B33 and S99B34 were the highest yielding of the translocation lines and similar in yield to Renville. These lines should be useful to breeders attempting to produce dual-purpose durum or for cereal chemists studying effects of Glu-D1d in a durum background.
Hexaploid triticale D-genome, disomic substitution lines. A partial set of 10 hexaploid triticale D-genome disomic substitution lines except for 2D(2A), 5D(5A), 3D(3B), and 5D(5B) were developed from crosses between Langdon durum D-genome disomic substitution lines and 'Gazelle' rye (Table 3). The triticale substitution lines 4D(4A) and 6D(6B) were produced from colchicine treatment of F1s and other eight lines were selected from partially fertile F1s. Most of the triticale D-genome substitutions had reduced seed fertility except that 1D(1A), 1D(1B), and 7D(7B) substitutions had the same high level of fertility as the LDN triticale. Because these hexaploid triticale D-genome disomic substitutions have a uniform genetic background, they could be used to evaluate the effects of each of the D-genome chromosomes on economically important traits of hexaploid triticale, such as grain shriveling, seed quality, and productivity.
| Line No. | Pedigree | Source of Ae. tauschii |
|---|---|---|
| 1 | Langdon/Ae. tauschii CIae 1 | NSGC, Aberdeen, Idaho |
| 2 | Langdon/Ae. tauschii CIae 5 | NSGC, Aberdeen, Idaho |
| 3 | Langdon/Ae. tauschii CIae 9 | NSGC, Aberdeen, Idaho |
| 4 | Langdon/Ae. tauschii CIae 11 | NSGC, Aberdeen, Idaho |
| 5 | Langdon/Ae. tauschii CIae 14 | NSGC, Aberdeen, Idaho |
| 7 | Langdon/Ae. tauschii CIae 22 | NSGC, Aberdeen, Idaho |
| 8 | Langdon/Ae. tauschii CIae 25 | NSGC, Aberdeen, Idaho |
| 9 | Langdon/Ae. tauschii CIae 26 | NSGC, Aberdeen, Idaho |
| 10 | Langdon/Ae. tauschii H80-101-4 | Haifa, Israel |
| 11 | Langdon/Ae. tauschii H80-114-1 | Haifa, Israel |
| 12 | Langdon/Ae. tauschii H80-115-3 | Haifa, Israel |
| 13 | Langdon/Ae. tauschii PI 220331 | NSGC, Aberdeen, Idaho |
| 14 | Langdon/Ae. tauschii PI 220641 | NSGC, Aberdeen, Idaho |
| 15 | Langdon/Ae. tauschii PI 317392 | NSGC, Aberdeen, Idaho |
| 16 | Langdon/Ae. tauschii RL 5003 | Winnipeg, Manitoba, Canada |
| 17 | Langdon/Ae. tauschii RL 5214 | Winnipeg, Manitoba, Canada |
| 19 | Langdon/Ae. tauschii RL 5259 | Winnipeg, Manitoba, Canada |
| 20 | Langdon/Ae. tauschii RL 5261 | Winnipeg, Manitoba, Canada |
| 21 | Langdon/Ae. tauschii RL 5263 | Winnipeg, Manitoba, Canada |
| 22 | Langdon/Ae. tauschii RL 5266-1 | Winnipeg, Manitoba, Canada |
| 23 | Langdon/Ae. tauschii RL 5271 | Winnipeg, Manitoba, Canada |
| 24 | Langdon/Ae. tauschii RL 5272 | Winnipeg, Manitoba, Canada |
| 25 | Langdon/Ae. tauschii RL 5286 | Winnipeg, Manitoba, Canada |
| 26 | Langdon/Ae. tauschii RL 5392 | Winnipeg, Manitoba, Canada |
| 27 | Langdon/Ae. tauschii RL 5393 | Winnipeg, Manitoba, Canada |
| 28 | Langdon/Ae. tauschii RL 5492 | Winnipeg, Manitoba, Canada |
| 29 | Langdon/Ae. tauschii RL 5498 | Winnipeg, Manitoba, Canada |
| 30 | Langdon/Ae. tauschii RL 5527 | Winnipeg, Manitoba, Canada |
| 32 | Langdon/Ae. tauschii RL 5532 | Winnipeg, Manitoba, Canada |
| 34 | Langdon/Ae. tauschii RL 5544 | Winnipeg, Manitoba, Canada |
| 35 | Langdon/Ae. tauschii RL 5552 | Winnipeg, Manitoba, Canada |
| 36 | Langdon/Ae. tauschii RL 5555 | Winnipeg, Manitoba, Canada |
| 37 | Langdon/Ae. tauschii RL 5557 | Winnipeg, Manitoba, Canada |
| 38 | Langdon/Ae. tauschii RL 5560 | Winnipeg, Manitoba, Canada |
| 39 | Langdon/Ae. tauschii RL 5561 | Winnipeg, Manitoba, Canada |
| 40 | Langdon/Ae. tauschii RL 5562 | Winnipeg, Manitoba, Canada |
| 41 | Langdon/Ae. tauschii RL 5570 | Winnipeg, Manitoba, Canada |
| 44 | Langdon/Ae. tauschii PI 476874 | NSGC, Aberdeen, Idaho |
| 52 | Langdon/Ae. tauschii CIae 17 | NSGC, Aberdeen, Idaho |
| 53 | Langdon/Ae. tauschii PI 268210 | NSGC, Aberdeen, Idaho |
| 55 | Langdon/Ae. tauschii RL 5257 | Winnipeg, Manitoba, Canada |
| 56 | Langdon/Ae. tauschii RL 5258 | Winnipeg, Manitoba, Canada |
| 57 | Langdon/Ae. tauschii RL 5270 | Winnipeg, Manitoba, Canada |
| 58 | Langdon/Ae. tauschii AL8/78 | Zurich, Switzerland |
| 59 | Langdon/Ae. tauschii CIae 19 | NSGC, Aberdeen, Idaho |