Endemic and panglobal genetic groups, and divergence of host-associated forms in worldwide collections of the wheat leaf rust fungus Puccinia triticina as determined by genotyping by sequencing.

The wheat leaf rust fungus, Puccinia triticina, is found in the major wheat growing regions of the world and is a leading cause of yield loss in wheat. Populations of P. triticina are highly variable for virulence to resistance genes in wheat and adapt quickly to resistance genes in wheat cultivars. The objectives of this study were to determine the genetic relatedness of worldwide collections of P. triticina using restriction site associated genotyping by sequencing. A total of 558 isolates of P. triticina from wheat producing regions in North America, South America, Europe, the Middle East, Ethiopia, Russia, Pakistan, Central Asia, China, New Zealand, and South Africa were characterized at 6745 single nucleotide loci. Isolates were also tested for virulence to 20 near-isogenic lines that differ for leaf rust resistance genes. Populations that were geographically proximal were also more closely related for genotypes. In addition, groups of isolates within regions that varied for genotype were similar to groups from other regions, which indicated past and recent migration across regions. Isolates from tetraploid durum wheat in five different regions were highly related with distinct genotypes compared to isolates from hexaploid common wheat. Based on a molecular clock, isolates from durum wheat found only in Ethiopia were the first to diverge from a common ancestor form of P. triticina that is found on the wild wheat relative Aegilops speltoides, followed by the divergence of isolates found worldwide that are virulent to durum wheat, and then by isolates found on common wheat.

Multilocus Genotypes of the Wheat Leaf Rust Fungus Puccinia triticina in Worldwide Regions Indicate Past and Current Long-Distance Migration.

Many plant pathogenic fungi have a global distribution across diverse ecological zones and agricultural production systems. Puccinia triticina, the wheat leaf rust fungus, is a major pathogen in many wheat production areas of the world. The objective of this research was to determine the genetic relatedness of P. triticina in different worldwide regions. A total of 831 single-uredinial isolates collected from 11 regions were characterized for multilocus genotype at 23 simple sequence repeat loci and for virulence to 20 lines of wheat with single genes for leaf rust resistance. A total of 424 multilocus genotypes and 497 virulence phenotypes were found. All populations had high heterozygosity and significant correlation between virulence and molecular variation, which indicated clonal reproduction. The populations from North America and South America, Central Asia and Russia, and the Middle East and Europe were closely related for multilocus genotypes and many individual isolates from other continental regions were closely related. Twenty-seven multilocus genotypes were found in more than one continental region, and 13 of these had isolates with identical virulence phenotypes. The wide geographic distribution of identical and highly related multilocus genotypes of P. triticina indicated past and more recent migration events facilitated by the spread of clonally produced urediniospores.

Mitochondrial epileptic encephalopathy, 3-methylglutaconic aciduria and variable complex V deficiency associated with TIMM50 mutations.

Mitochondrial encephalopathies are a heterogeneous group of disorders that, usually carry grave prognosis. Recently a homozygous mutation, Gly372Ser, in the TIMM50 gene, was reported in an abstract form, in three sibs who suffered from intractable epilepsy and developmental delay accompanied by 3-methylglutaconic aciduria. We now report on four patients from two unrelated families who presented with severe intellectual disability and seizure disorder, accompanied by slightly elevated lactate level, 3-methylglutaconic aciduria and variable deficiency of mitochondrial complex V. Using exome analysis we identified two homozygous missense mutations, Arg217Trp and Thr252Met, in the TIMM50 gene. The TIMM50 protein is a subunit of TIM23 complex, the mitochondrial import machinery. It serves as the major receptor in the intermembrane space, binding to proteins which cross the mitochondrial inner membrane on their way to the matrix. The mutations, which affected evolutionary conserved residues and segregated with the disease in the families, were neither present in large cohorts of control exome analyses nor in our ethnic specific exome cohort. Given the phenotypic similarity, we conclude that missense mutations in TIMM50 are likely manifesting by severe intellectual disability and epilepsy accompanied by 3-methylglutaconic aciduria and variable mitochondrial complex V deficiency. 3-methylglutaconic aciduria is emerging as an important biomarker for mitochondrial dysfunction, in particular for mitochondrial membrane defects.

Microcephaly, intractable seizures and developmental delay caused by biallelic variants in TBCD: further delineation of a new chaperone-mediated tubulinopathy.

Microtubule dynamics play a crucial role in neuronal development and function, and several neurodevelopmental disorders have been linked to mutations in genes encoding tubulins and functionally related proteins. Most recently, variants in the tubulin cofactor D (TBCD) gene, which encodes one of the five co-chaperones required for assembly and disassembly of α/ß-tubulin heterodimer, were reported to underlie a recessive neurodevelopmental/neurodegenerative disorder. We report on five patients from three unrelated families, who presented with microcephaly, intellectual disability, intractable seizures, optic nerve pallor/atrophy, and cortical atrophy with delayed myelination and thinned corpus callosum on brain imaging. Exome sequencing allowed the identification of biallelic variants in TBCD segregating with the disease in the three families. TBCD protein level was significantly reduced in cultured fibroblasts from one patient, supporting defective TBCD function as the event underlying the disorder. Such reduced expression was associated with accelerated microtubule re-polymerization. Morpholino-mediated TBCD knockdown in zebrafish recapitulated several key pathological features of the human disease, and TBCD overexpression in the same model confirmed previous studies documenting an obligate dependency on proper TBCD levels during development. Our findings confirm the link between inactivating TBCD variants and this newly described chaperone-associated tubulinopathy, and provide insights into the phenotype of this disorder.

A New Rust Disease on Wild Coffee (Psychotria nervosa) Caused by Puccinia mysuruensis sp. nov.

Psychotria nervosa, commonly called "wild coffee" (Rubiaceae), is an important ethno-medicinal plant in India. In 2010, a new rust disease of P. nervosa was observed in three regions of Mysore District, Karnataka (India), with disease incidence ranging from 58 to 63%.Typical symptoms of the rust disease on wild coffee were prominently visible during the early monsoon season (May to June), with chlorotic spots on the adaxial and black pustules (telia) on the abaxial leaf surface. Telia produced abundant teliospores, which were bicelled, pedicillate, and measured 33 to 45 by 19 to 30 µm. The germination of teliospores produced a typical metabasidium bearing four basidiospores, each containing two haploid nuclei. Spore stages of the wild coffee rust pathogen were studied using artificially inoculated healthy wild coffee plants with germinated teliospores. Only telia were observed on the inoculated plants, indicating that this rust fungus has an abbreviated microcyclic life cycle that includes only teliospores and basidiospores. Phylogenetic analysis based on internal transcribed spacer and partial large subunit (LSU) sequence data showed that the wild coffee rust pathogen is related to Macruropyxis fraxini, Puccinia bartholomaei, P. choridis, and P. sparganioidis. The herbarium sample of P. psychotriae was examined and was shown to be different with respect to telium size and teliospore dimensions (24 to 32 by 13 to 18 µm). Therefore, the rust pathogen causing wild coffee rust is a new species, P. mysuruensis sp. nov.

SLC1A4 mutations cause a novel disorder of intellectual disability, progressive microcephaly, spasticity and thin corpus callosum.

Two unrelated patients, presenting with significant global developmental delay, severe progressive microcephaly, seizures, spasticity and thin corpus callosum (CC) underwent trio whole-exome sequencing. No candidate variant was found in any known genes related to the phenotype. However, crossing the data of the patients illustrated that they both manifested pathogenic variants in the SLC1A4 gene which codes the ASCT1 transporter of serine and other neutral amino acids. The Ashkenazi patient is homozygous for a deleterious missense c.766G>A, p.(E256K) mutation whereas the Ashkenazi-Iraqi patient is compound heterozygous for this mutation and a nonsense c.945delTT, p.(Leu315Hisfs*42) mutation. Structural prediction demonstrates truncation of significant portion of the protein by the nonsense mutation and speculates functional disruption by the missense mutation. Both mutations are extremely rare in general population databases, however, the missense mutation was found in heterozygous mode in 1:100 Jewish Ashkenazi controls suggesting a higher carrier rate among Ashkenazi Jews. We conclude that SLC1A4 is the disease causing gene of a novel neurologic disorder manifesting with significant intellectual disability, severe postnatal microcephaly, spasticity and thin CC. The role of SLC1A4 in the serine transport from astrocytes to neurons suggests a possible pathomechanism for this disease and implies a potential therapeutic approach.

The neuropsychological profile of patients with 3-methylglutaconic aciduria type III, Costeff syndrome.

Costeff syndrome is a rare genetic neuro-ophthalmological syndrome consisting of early-onset bilateral optic atrophy along with a progressive complex motor disorder with elevated levels of urinary 3-methylglutaconic acid and 3-methylglutaric acid. While borderline to mild cognitive deficits have been considered to be common in patients with this syndrome, a comprehensive cognitive assessment has never been performed. The aim of the current study was to explore the cognitive profile associated with Costeff syndrome. Sixteen adult patients diagnosed with Costeff syndrome were administered a neuropsychological test battery that was composed of standardized verbal tests adapted for the blind. General intelligence ranged from average to borderline, with a group mean consistent with intact general cognitive functioning (VIQmean = 85, z = -1) in the low-average range of the general population. The auditory immediate and delayed memory indexes were in the average range and were significantly higher than the general cognitive functioning, whereas the working memory index was significantly lower than the general cognitive functioning. Adult patients with Costeff syndrome have intact global cognition and learning abilities and strong auditory memory performance. © 2015 Wiley Periodicals, Inc.

Mutation of a new gene causes a unique form of Hermansky-Pudlak syndrome in a genetic isolate of central Puerto Rico.

Hermansky-Pudlak syndrome (HPS) is a rare autosomal recessive disorder characterized by oculocutaneous albinism and a storage pool deficiency due to an absence of platelet dense bodies. Lysosomal ceroid lipofuscinosis, pulmonary fibrosis and granulomatous colitis are occasional manifestations of the disease. HPS occurs with a frequency of one in 1800 in north-west Puerto Rico due to a founder effect. Several non-Puerto Rican patients also have mutations in HPS1, which produces a protein of unknown function. Another gene, ADTB3A, causes HPS in the pearl mouse and in two brothers with HPS-2 (refs. 11,12). ADTB3A encodes a coat protein involved in vesicle formation, implicating HPS as a disorder of membrane trafficking. We sought to identify other HPS-causing genes. Using homozygosity mapping on pooled DNA of 6 families from central Puerto Rico, we localized a new HPS susceptibility gene to a 1.6-cM interval on chromosome 3q24. The gene, HPS3, has 17 exons, and a putative 113.7-kD product expected to reveal how new vesicles form in specialized cells. The homozygous, disease-causing mutation is a large deletion and represents the second example of a founder mutation causing HPS on the small island of Puerto Rico. We also present an allele-specific assay for diagnosing individuals heterozygous or homozygous for this mutation.

Genetic differentiation of Puccinia triticina populations in the Middle East and genetic similarity with populations in Central Asia.

Leaf rust of wheat, caused by Puccinia triticina, is a common and widespread disease in the Middle East. The objective of this study was to determine whether genetically differentiated groups of P. triticina are present in the Middle East region and to compare the population from the Middle East with the previously characterized population from Central Asia to determine whether genetically similar groups of isolates are found in the two regions. In total, 118 isolates of P. triticina collected from common wheat and durum wheat in Egypt, Israel, Turkey, Ethiopia, and Kenya were tested for virulence on 20 lines of wheat with single genes for leaf rust resistance and for molecular genotypes with 23 simple-sequence repeat (SSR) markers. After removal of isolates with identical virulence and SSR genotype in each country, 103 isolates were retained for further analysis. Clustering of SSR genotypes based on two-dimensional principal coordinates and virulence to wheat differential lines grouped the isolates into four Middle East (ME) groups. The two largest ME groups had virulence phenotypes typical of isolates collected from common wheat and two smaller ME groups had virulence typical of isolates collected from durum wheat. All pairs of ME groups were significantly differentiated for SSR genotype based on R(ST) and F(ST) statistics, and for virulence phenotype based on Φ(PT). All ME groups had observed values of heterozygosity greater than expected and significant fixation indices that indicated the clonal reproduction of urediniospores in the overall population. Linkage disequilibria for SSR genotypes was high across the entire population. The overall values of R(ST) and F(ST) were lower when isolates were grouped by country of origin that indicated the likely migration of isolates within the region. Although the two ME groups with virulence typical of isolates from common wheat were not differentiated for SSR genotype from groups of isolates from Central Asia based on R(ST), there was no direct evidence for migration between the two regions because all ME isolates differed from the Central Asia isolates for SSR genotypes.

Glyceryl triacetate for Canavan disease: a low-dose trial in infants and evaluation of a higher dose for toxicity in the tremor rat model.

Canavan disease (CD) is a fatal dysmyelinating genetic disorder associated with aspartoacylase deficiency, resulting in decreased brain acetate levels and reduced myelin lipid synthesis in the developing brain. Here we tested tolerability of a potent acetate precursor, glyceryl triacetate (GTA), at low doses in two infants diagnosed with CD, aged 8 and 13 months. Much higher doses of GTA were evaluated for toxicity in the tremor rat model of CD. GTA was given orally to the infants for up to 4.5 and 6 months, starting at 25 mg/kg twice daily, doubling the dose weekly until a maximum of 250 mg/kg reached. Wild-type and tremor rat pups were given GTA orally twice daily, initially at a dose of 4.2 g/kg from postnatal days 7 through 14, and at 5.8 g/kg from day 15 through 23, and thereafter in food (7.5%) and water (5%). At the end of the trial (approximately 90 to 120 days) sera and tissues from rats were analysed for changes in blood chemistry and histopathology. GTA treatment caused no detectable toxicity and the patients showed no deterioration in clinical status. In the high-dose animal studies, no significant differences in the mean blood chemistry values occurred between treated and untreated groups, and no lesions indicating toxicity were detectable in any of the tissues examined. Lack of GTA toxicity in two CD patients in low-dose trials, as well as in high-dose animal studies, suggests that higher, effective dose studies in human CD patients are warranted.

Genetics of resistance to wheat leaf rust, stem rust, and powdery mildew in Aegilops sharonensis.

Aegilops sharonensis (Sharon goatgrass) is a wild relative of wheat and a rich source of genetic diversity for disease resistance. The objectives of this study were to determine the genetic basis of leaf rust, stem rust, and powdery mildew resistance in A. sharonensis and also the allelic relationships between genes controlling resistance to each disease. Progeny from crosses between resistant and susceptible accessions were evaluated for their disease reaction at the seedling and/or adult plant stage to determine the number and action of genes conferring resistance. Two different genes conferring resistance to leaf rust races THBJ and BBBB were identified in accessions 1644 and 603. For stem rust, the same single gene was found to confer resistance to race TTTT in accessions 1644 and 2229. Resistance to stem rust race TPMK was conferred by two genes in accessions 1644 and 603. A contingency test revealed no association between genes conferring resistance to leaf rust race THBJ and stem rust race TTTT or between genes conferring resistance to stem rust race TTTT and powdery mildew isolate UM06-01, indicating that the respective resistance genes are not linked. Three accessions (1644, 2229, and 1193) were found to carry a single gene for resistance to powdery mildew. Allelism tests revealed that the resistance gene in accession 1644 is different from the respective single genes present in either 2229 or 1193. The simple inheritance of leaf rust, stem rust, and powdery mildew resistance in A. sharonensis should simplify the transfer of resistance to wheat in wide crosses.

Mutations in AIFM1 cause an X-linked childhood cerebellar ataxia partially responsive to riboflavin.

BACKGROUND: AIFM1 encodes a mitochondrial flavoprotein with a dual role (NADH oxidoreductase and regulator of apoptosis), which uses riboflavin as a cofactor. Mutations in the X-linked AIFM1 were reported in relation to two main phenotypes: a severe infantile mitochondrial encephalomyopathy and an early-onset axonal sensorimotor neuropathy with hearing loss. In this paper we report two unrelated males harboring AIFM1 mutations (one of which is novel) who display distinct phenotypes including progressive ataxia which partially improved with riboflavin treatment. METHODS: For both patients trio whole exome sequencing was performed. Validation and segregation were performed with Sanger sequencing. Following the diagnosis, patients were treated with up to 200 mg riboflavin/day for 12 months. Ataxia was assessed by the ICARS scale at baseline, and 6 and 12 months following treatment. RESULTS: Patient 1 presented at the age of 5 years with auditory neuropathy, followed by progressive ataxia, vermian atrophy and axonal neuropathy. Patient 2 presented at the age of 4.5 years with severe limb and palatal myoclonus, followed by ataxia, cerebellar atrophy, ophthalmoplegia, sensorineural hearing loss, hyporeflexia and cardiomyopathy. Two deleterious missense mutations were found in the AIFM1 gene: p. Met340Thr mutation located in the FAD dependent oxidoreductase domain and the novel p. Thr141Ile mutation located in a highly conserved DNA binding motif. Ataxia score, decreased by 39% in patient 1 and 20% in patient 2 following 12 months of treatment. CONCLUSION: AIFM1 mutations cause childhood cerebellar ataxia, which may be partially treatable in some patients with high dose riboflavin.

Peak bone mass in patients with phenylketonuria.

OBJECTIVE: Several studies have suggested a compromised bone mass in phenylketonuria patients but most reported on heterogeneous or small patient groups. Our aim was to evaluate peak bone mass in adult PKU patients and to relate BMD to nutritional parameters. PATIENTS AND METHODS: BMD was measured by dual-energy x-ray absorptiometry in 31 adult PKU patients (18 female), mean age 25 +/- 5.3 years. Nutritional intake was calculated based on food diaries. Diet adherence was determined based on patients' report. RESULTS: Mean blood phenylalanine (Phe) concentration was 968 +/- 526 micromol/L (16 +/- 8.7 mg/dl). Eight patients (32.2%) met the recommended blood Phe concentration of <726 micromol/L (<12 mg/dl), and there was no significant difference in Phe concentrations between diet-adherent and non-adherent patients. Osteopenia was detected in 11 patients (38.7%), while osteoporosis was detected in 2 patients (6.5%). No correlation was found between BMD and age, blood minerals, Phe, vitamin D and alkaline phosphatase levels, calcium and protein intake, body mass index, and body fat percentage. CONCLUSIONS: Peak bone mass is decreased in PKU patients. Possible explanations include long-standing dietary deficiency in protein, calcium, vitamin D or trace elements, or a primary defect in bone turnover inherent to the disease itself. Our data do not favour any of these hypotheses. Further studies are needed to elucidate the cause of low bone density in PKU patients.

Resistance of Sharon Goatgrass (Aegilops sharonensis) to Fungal Diseases of Wheat.

Sharon goatgrass (Aegilops sharonensis) is a wild relative of wheat that is native to Israel and Lebanon. The importance of A. sharonensis as a source of new resistance genes for wheat warrants additional research on the characterization of accessions for economically important genes. Thus, the objectives of this study were to evaluate a collection of A. sharonensis accessions for resistance to seven important fungal diseases of wheat and assess the phenotypic diversity of the germplasm for disease reaction. The frequency of resistance in A. sharonensis was highest to powdery mildew (79 to 83%) and leaf rust (60 to 77%). Resistance to stem rust also was common, although the percentage of resistant accessions varied markedly depending on the pathogen race-from 13% to race TTTT to 72% to race QCCJ. The frequency of resistance was intermediate to stripe rust (45%) and low to tan spot (15 to 29%) and spot blotch (0 to 34%). None of the A. sharonensis accessions was resistant to Fusarium head blight. Many of the accessions tested exhibited heterogeneous reactions (i.e., had both resistant and susceptible plants) to one or more of the diseases, suggesting that heterozygosity may be present at some resistance loci. Substantial variation was observed in the level of diversity to individual diseases because Shannon's Equitability index ranged from 0.116 (for Fusarium head blight) to 0.994 (for tan spot). A high level of diversity was found both between and within collection sites. Moreover, differences in the geographic distribution of resistant accessions were observed. For example, accessions from northern Israel generally were less diverse and less resistant to leaf rust and stripe rust than accessions from more southern locations. Four A. sharonensis accessions were highly resistant to most of the diseases evaluated and may provide a source of unique resistance genes for introgression into cultivated wheat.

Creatine transporter deficiency: Novel mutations and functional studies.

X-linked cerebral creatine deficiency (MIM 300036) is caused by deficiency of the creatine transporter encoded by the SLC6A8 gene. Here we report three patients with this condition from Israel. These unrelated patients were evaluated for global developmental delays and language apraxia. Borderline microcephaly was noted in one of them. Diagnosis was prompted by brain magnetic resonance imaging and spectroscopy which revealed normal white matter distribution, but absence of the creatine peak in all three patients. Biochemical testing indicated normal plasma levels of creatine and guanidinoacetate, but an increased urine creatine/creatinine ratio. The diagnosis was confirmed by demonstrating absent ([14])C-creatine transport in fibroblasts. Molecular studies indicated that the first patient is hemizygous for a single nucleotide change substituting a single amino acid (c.619 C > T, p.R207W). Expression studies in HeLa cells confirmed the causative role of the R207W substitution. The second patient had a three base pair deletion in the SLC6A8 gene (c.1222_1224delTTC, p.F408del) as well as a single base change (c.1254 + 1G > A) at a splicing site in the intron-exon junction of exon 8, the latter occurring de novo. The third patient, had a three base pair deletion (c.1006_1008delAAC, p.N336del) previously reported in other patients with creatine transporter deficiency. These three patients are the first reported cases of creatine transporter deficiency in Israel.

Virulence associations in oat crown rust.

ABSTRACT Isolates of Puccinia coronata obtained from natural populations of Avena sterilis in Israel, winter oat (A. sativa) cultivars in Texas, and spring oat cultivars in the Northern Plains states of Minnesota, North Dakota, and South Dakota were analyzed for significance of pairwise virulence associations. Isolates from all three regions were tested on 25 oat lines with single P. coronata (Pc) genes for crown rust resistance from A. sterilis and one line with a Pc gene from A. sativa. Isolates from Israel were tested also on 11 Iowa backcross lines with undesignated crown rust resistance genes from A. sterilis. Four associated virulence groups were identified from significant positive virulence associations that were consistent across all three regions. Group 38 included virulence to Pc-38, Pc-39, Pc-55, Pc-63, and Pc-71; group 45 included virulence to Pc-45, Pc-46, Pc-48, Pc-52, Pc-54, and Pc-57; group 58 included virulence to Pc-35, Pc-40, Pc-58, and Pc-59; and group 61 included virulence to Pc- 36, Pc-51, Pc-56, Pc-60, and Pc-61. Virulence to Pc-70 showed the strongest association to virulences in group 38 but also showed significant association with virulence to Pc-45, Pc-35, and Pc-58. Virulences in group 61 were consistently negatively associated with virulences in group 38 in each region. In Israel, virulences to five of the Iowa lines showed positive associations to virulences in group 61 and negative associations to virulences in groups 38 and 45. Close similarity of reactions of nearly all isolates to Pc-39, Pc-55, and Pc-71 suggest that these genes may be identical or nearly identical alleles.

Spore dimensions of Puccinia species of cereal hosts as determined by image analysis.

Digital image analysis was used to measure dimensions of spores produced by Puccinia coronata, P. graminis, P. hordei, P. recondita, P. striiformis and P. triticina. Included were teliospores, basidiospores, urediniospores and, except for P. striiformis, pycniospores and aeciospores. Length, width and projection area of spores were measured with NIH Image or Scion software. By using limits on size, spores were automatically selected and measured, except for teliospores, which required manual elimination of the pedicel and separation of images of adhering spores. Length and width were determined as the major and minor axes of the best fitting ellipse for each spore. This procedure gave values for length and width close to results obtained with an ocular micrometer. Projection area was determined as the number of pixels within spore boundaries multiplied by the area represented by each pixel, giving values that are not feasible to obtain accurately with an ocular micrometer. Of the species studied, spores of P. recondita had the largest dimensions, P. triticina had the smallest. The rank of the six species based on increasing width, length or projection area was almost the same, using each spore type except pycniospores. Generally, differences of 5% in a given spore dimension between two species were significant. Differences between species were greater with basidiospores and aeciospores than with other spore types. Teliospores were unique in that length and width were negatively correlated, resulting in less variation in area than in length or width. The results indicate that image analysis is useful for measuring spore dimensions, that projection area of spores is a useful added parameter for characterizing rust species and that dimensions of teliospores, basidiospores, aeciospores and urediniospores each are potentially useful for differentiating species.

Leaf Rust and Stem Rust Resistance in Triticum dicoccoides Populations in Israel.

A total of 742 single plant accessions of Triticum dicoccoides were collected from 26 locations in Israel. All accessions were evaluated for leaf rust (Puccinia triticina) resistance in field plots at Tel Aviv, and subsets of 284 and 468 accessions were tested in the greenhouse in Tel Aviv and St. Paul, MN, respectively, for seedling resistance to leaf rust; 460 accessions were also tested for seedling resistance to stem rust (Puccinia graminis f. sp. tritici) in St. Paul. One accession was highly resistant to leaf rust in seedling tests in Tel Aviv, and 21 others had moderately susceptible to moderately resistant seedling resistance. Four accessions were highly resistant to leaf rust in seedling tests in St. Paul, and 11 were resistant to at least one stem rust race. Adult resistance to leaf rust was more common than seedling resistance among the accessions; 21 accessions had less than 25% leaf rust severity in field plots compared with 80 to 90% severity for highly susceptible accessions. Most of the accessions with effective adult plant resistance came from two nearby locations in Upper Galilee, a region where populations of T. dicoccoides are most extensive and genetically diverse. These accessions may provide valuable new partial resistance genes for durable protection against leaf rust in cultivated wheat.

Resistance to Leaf Rust, Stripe Rust, and Stem Rust in Aegilops spp. in Israel.

In all, 1,323 single plant accessions of Aegilops bicornis, A. kotschyi, A. longissima, A. ovata, A. searsii, A. sharonensis, A. speltoides, and A. variabilis collected from 18 regions in Israel and 2 adjacent regions in Lebanon and Egypt were evaluated for leaf rust (Puccinia triticina) and stripe rust (P. striiformis) resistance in field plots and for seedling resistance to leaf rust and stem rust (P. graminis f. sp. tritici) in greenhouse tests. Nearly all accessions of A. speltoides were highly resistant to leaf rust, stripe rust, and stem rust. A. longissima and A. ovata were highly resistant to stripe rust, whereas A. bicornis and A. kotschyi were highly susceptible. A. searsii was highly susceptible to stem rust, but 24 to 51% of accessions of A. bicornis, A. longissima, A. ovata, and A. variabilis were resistant to stem rust. Except for A. ovata and A. speltoides, more than 95% of the Aegilops accessions were susceptible to leaf rust caused by P. recondita alternating on Anchusa spp. Only Aegilops ovata was susceptible to P. recondita from Echium spp. A. bicornis, A. koschyi, and A. searsii were highly susceptible as seedlings to common wheat leaf rust caused by P. triticina. Most accessions of A. variabilis and about half of the accessions of A. longissima had good seedling resistance to P. triticina. Few accessions of A. ovata showed seedling resistance to the P. triticina population in Israel, but 30% were resistant to U.S. isolates. In field tests, A. bicornis showed high susceptibility to common wheat leaf rust, but more than 90% of the accessions of the other Aegilops spp. developed little or no leaf rust on adult plants. The Aegilops spp. in Israel and adjoining countries provide a rich and varied source of rust resistance for wheat breeding.