Resistance to recombinant stem rust race TPPKC in hard red spring 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.     

A robust molecular marker for the detection of shortened introgressed segment carrying the stem rust resistance gene <Emphasis Type="Italic">Sr22</Emphasis> in common wheat

Stem rust resistance gene Sr22 transferred to common wheat from Triticum boeoticum and T. monococcum remains effective against commercially prevalent pathotypes of Puccinia graminis f. sp. tritici, including Ug99 and its derivatives. Sr22 was previously located on the long arm of chromosome 7A. Several backcross derivatives (hexaploid) possessing variable sized Sr22-carrying segments were used in this study to identify a closely linked DNA marker. Expressed sequenced tags belonging to the deletion bin 7AL-0.74–0.86, corresponding to the genomic location of Sr22 were screened for polymorphism. In addition, RFLP markers that mapped to this region were targeted. Initial screening was performed on the resistant and susceptible DNA bulks obtained from backcross derivatives carrying Sr22 in three genetic backgrounds with short T. boeoticum segments. A cloned wheat genomic fragment, csIH81, that detected RFLPs between the resistant and susceptible bulks, was converted into a sequence tagged site (STS) marker, named cssu22. Validation was performed on Sr22 carrying backcross-derivatives in fourteen genetic backgrounds and other genotypes used for marker development. Marker cssu22 distinguished all backcross-derivatives from their respective recurrent parents and co-segregated with Sr22 in a Schomburgk (+Sr22)/Yarralinka (−Sr22)-derived recombinant inbred line (RIL) population. Sr22 was also validated in a second population, Sr22TB/Lakin-derived F₄ selected families, containing shortened introgressed segments that showed recombination with previously reported flanking microsatellite markers.     

Identification of a STS marker linked to the Aegilops speltoides-derived leaf rust resistance gene Lr28 in wheat

 A sequence-tagged-site (STS) marker is reported linked to Lr28, a leaf rust resistance gene in wheat. RAPD (random amplified polymorphic DNA) analysis of near-isogenic lines (NILs) of Lr28 in eight varietal backgrounds was carried out using random primers. Genomic DNA enriched for low-copy sequences was used for RAPD analysis to overcome the lack of reproducibility due to the highly repetitive DNA sequences present in wheat. Of 80 random primers tested on the enriched DNA, one RAPD marker distinguished the NILs and the donor parent from the susceptible recurrent parents. The additional band present in resistant lines was cloned, sequenced, and STS primers specific for Lr28 were designed. The STS marker (Indian patent pending: 380 Del98) was further confirmed by bulk segregation analysis of F₃ families. It was consistently present in the NILs, the resistant F₃ bulk and the resistant F₃ lines, but was absent in recurrent parents, the susceptible F₃ bulk and the susceptible F₃ lines. Received: 20 February 1998 / Accepted: 4 March 1998     

A region of barley chromosome 6H harbors multiple major genes associated with net type net blotch resistance

Net type net blotch (NTNB), caused by Pyrenophora teres f. teres Drechs., is prevalent in barley growing regions worldwide. A population of 118 doubled haploid (DH) lines developed from a cross between barley cultivars ‘Rika’ and ‘Kombar’ were used to evaluate resistance to NTNB due to their differential reaction to various isolates of P. teres f. teres. Rika was resistant to P. teres f. teres isolate 15A and susceptible to isolate 6A. Conversely, Kombar was resistant to 6A, but susceptible to 15A. A progeny isolate of a 15A × 6A cross identified as 15A × 6A#4 was virulent on both parental lines. The Rika/Kombar (RK) DH population was evaluated for disease reactions to the three isolates. Isolate 15A induced a resistant:susceptible ratio of 78:40 (R:S) whereas isolate 6A induced a resistant:susceptible ratio of 40:78. All but two lines had opposite disease reactions indicating two major resistance genes linked in repulsion. Progeny isolate 15A × 6A#4 showed a resistant:susceptible ratio of 1:117 with the one resistant line also being the single line that was resistant to both 15A and 6A. An RK F₂ population segregated in a 1:3 (R:S) ratio for both 15A and 6A indicating that resistance is recessive. Molecular markers were used to identify a region on chromosome 6H that harbors the two NTNB resistance genes. This work shows that multiple NTNB resistance genes exist at the locus on chromosome 6H, and the recombinant DH line harboring the resistance alleles from both parents will be useful for the development of NTNB-resistant barley germplasm.     

ROSA26 mice carry a modifier of Min-induced mammary and intestinal tumor development

B6.129S7-Gtrosa26 (B6.R26) mice carry a LacZ-neoR insertion on Chromosome (Chr) 6, made by promoter trapping with 129 ES cells. Female C57BL/6J Apc ^Min /+ (B6Min/+) mice are highly susceptible to intestinal tumors and to the induction of mammary tumors after treatment with ethylnitrosourea (ENU). However, B6.R26/+Min/+ females develop fewer mammary and intestinal tumors after ENU treatment than do B6 Min/+ mice. B6.R26/+ mice from two independently derived congenic lines show this modifier effect. Each of these congenic lines carries approximately 20 cM of 129-derived DNA flanking the insertion, raising the possibility that the resistance is due to a linked modifier locus. To further map the modifier locus, we have generated several lines of mice carrying different regions of the congenic interval. We have found that resistance to mammary and intestinal tumors in ENU-treated Min/+ mice maps to a minimum 4-cM interval that includes the ROSA26 LacZ-neoR insertion. Therefore, the resistance to tumor development is due to either the ROSA26 insertion or a very tightly linked modifier locus. Received: 10 May 2000 / Accepted: 25 July 2000     

Inheritance of resistance to Yam mosaic virus, genus Potyvirus, in white yam (Dioscorea rotundata)

Yam mosaic virus (YMV) causes the most-widespread and economically important viral disease affecting white yam (Dioscorea rotundata) in West Africa. The genetic basis of resistance in white yam to a Nigerian isolate of YMV was investigated in three tetraploid D. rotundata genotypes: TDr 93–1, TDr 93–2 and TDr 89/01444. F₁ progeny were produced using TDr 87/00571 and TDr 87/00211 as the susceptible parents. Segregation ratios indicated that a single dominant gene in a simplex condition governs the resistance in TDr 89/01444, while the resistance in TDr 93–2 is associated with the presence of a major recessive gene in duplex configuration. Segregation of progeny of the cross TDr 93–1×TDr 87/00211 fitted a genetic ratio of 2.48:1 resistant:susceptible, which can be expected when two simplex heterozygotes are crossed, indicating the possible modifying effect of the susceptible parent. A triple antibody immunosorbent assay (TAS-ELISA) was used for virus detection in inoculated plants. Slight mosaic symptoms appeared on most resistant individuals, while asymptomatic resistant genotypes with high ELISA (A₄₀₅) values were observed in all crosses. Such a heterogeneous response suggests the influence of additional modifier genes that segregate in the progeny. The finding that resistance can be inherited as a dominant or recessive character has important implications for YMV resistance breeding. Received: 15 August 2000 / Accepted: 12 April 2001     

Nature and type of gene action governing resistance to Helminthosporium turcicum leaf blight in maize (Zea mays L.)

Six generations, consisting of three resistant parents, three susceptible parents, their 15 possible F₁ crosses, 15 F₂'s, 15 BC₁'s (F₁ x resistant female parent) and 15 BC₂'s (F₁ x susceptible male parent) were analysed following Hayman (Heredity 12: 371–390, 1958) to evaluate the nature and type of gene action governing resistance to H. turcicum. The results showed that all types of gene effects, viz., additive, dominance and epistasis (i.e., additive x additive, additive x dominance and dominance x dominance) were operating in one cross or the other in controlling resistance. However, it was additive gene action and dominance x dominance type of epistasis with duplicate nature that were important in controlling resistance in most crosses. Depending upon the final objectives, one of the breeding methods, viz., recurrent selection, heterosis breeding, back-cross method or full-sib selection (bi-parental mating) may be followed.     

Glutamate Receptor 6 Gene (<Emphasis Type="Italic">GluR6</Emphasis> or <Emphasis Type="Italic">GRIK2</Emphasis>) Polymorphisms in the Indian Population: A Genetic Association Study on Autism Spectrum Disorder

Autism is a neurodevelopmental disorder with early manifestation. It is a multifactorial disorder and several susceptible chromosomal regions for autism are identified through genome scan studies. The gene coding for glutamate receptor 6 (GluR6 or GRIK2) has been suggested as a candidate gene for autism based on its localization in the autism specific region on chromosome 6q21 and the involvement of receptor protein in cognitive functions like learning and memory. Despite its importance, so far no studies have been carried out on possible involvement of GluR6 with autism in the Indian population. Therefore in the present study, we have performed genetic analysis of three markers of GluR6 (SNP1: rs2227281, SNP2: rs2227283, SNP3: rs2235076) for possible association with autism through population, and family-based (TDT and HHRR) approaches. DSM-IV criteria and CARS/ADI-R have been utilized for diagnosis. Genotyping analysis for the SNPs has been carried out in 101 probands with autism spectrum disorder, 180 parents and 152 controls from different regions of India. Since the minor allele frequency of SNP3 was too low, the association studies have been carried out only for SNP1 and SNP2. Even though two earlier studies have shown association of these markers with autism, the present case–control and TDT, as well as HHRR analyses have not demonstrated any biased transmission of alleles or haplotypes to the affected offspring. Thus our results suggest that these markers of GluR6 are unlikely to be associated with autism in the Indian population.     

QTL analysis and mapping of pi21, a recessive gene for field resistance to rice blast in Japanese upland rice

Field resistance is defined as the resistance that allows effective control of a parasite under natural field conditions and is durable when exposed to new races of that parasite. To identify the genes for field resistance to rice blast, quantitative trait loci (QTLs) conferring field resistance to rice blast in Japanese upland rice were detected and mapped using RFLP and SSR markers. QTL analysis was carried out in F₄ progeny lines from the cross between Nipponbare (moderately susceptible, lowland) and Owarihatamochi (resistant, upland). Two QTLs were detected on chromosome 4 and one QTL was detected on each of chromosomes 9 and 12. The phenotypic variation explained by each QTL ranged from 7.9 to 45.7% and the four QTLs explained 66.3% of the total phenotypic variation. Backcrossed progeny lines were developed to transfer the QTL with largest effect using the susceptible cultivar Aichiasahi as a recurrent parent. Among 82 F₃ lines derived from the backcross, resistance segregated in the expected ratio of resistant 1 : heterozygous 2 : susceptible 1. The average score for blast resistance measured in the field was 4.2 ± 0.67, 7.5 ± 0.51and 8.2 ± 0.66, for resistant, heterozygous and susceptible groups, respectively. The resistance gene, designated pi21, was mapped on chromosome 4 as a single recessive gene between RFLP marker loci G271 and G317 at a distance of 5.0 cM and 8.5 cM, respectively. The relationship to previously reported major genes and QTLs conferring resistance to blasts, and the significance of marker-assisted selection to improve field resistance, are discussed. Received: 8 June 2000 / Accepted: 24 November 2000     

The ROSA26 LacZ-neo R insertion confers resistance to mammary tumors in Apc Min/+ mice

B6.129S7-Gtrosa26 (ROSA26) mice carry a LacZ-neo ^R insertion on Chromosome (Chr) 6, made by promoter trapping with AB1 129 ES cells. Female C57BL/6J Apc ^Min /+ (B6 Min/+) mice are very susceptible to the induction of mammary tumors after treatment with ethylnitrosourea (ENU). However, ENU-treated B6 mice carrying both Apc ^Min and ROSA26 are resistant to mammary tumor formation. Thus, ROSA26 mice carry a modifier of Min-induced mammary tumor susceptibility. We have previously mapped the modifier to a 4-cM interval of 129-derived DNA that also contains the ROSA26 insertion. Here we report additional evidence for the effect of the ROSA26 insertion on mammary tumor formation. To test the hypothesis that the resistance was due to a linked modifier locus, we utilized two approaches. We have derived and tested two lines of mice that are congenic for 129-derived DNA within the minimal modifier interval and show that they are as susceptible to mammary tumors as are B6 mice. Additionally, we analyzed a backcross population segregating for the insertion and show that mice carrying the insertion are more resistant to mammary tumor development than are mice not carrying the insertion. Thus, the resistance is not due to a 129-derived modifier allele, but must be due to the ROSA26 insertion. In addition, the effect of the ROSA26 insertion can be detected in a backcross population segregating for other mammary modifiers. Received: 29 December 2000 / Accepted: 4 April 2001     

Identification and validation of SSR markers linked to the stem rust resistance gene Sr6 on the short arm of chromosome 2D in wheat

The wheat stem rust resistance gene Sr6, present in several wheat cultivars, confers a high level of resistance against a wide range of races of Puccinia graminis f. sp. tritici. Resistance conferred by Sr6 is influenced by temperature, light intensity, and genetic background of the recipient genotype. Here, we report the identification and validation of molecular markers linked to Sr6 that can be used for the detection of this gene in wheat breeding programs. A mapping population of 136 F₂ plants and their F_2:3 families derived from a cross between near-isogenic lines, ‘Chinese Spring’ and ISr6-Ra, were screened for stem rust reaction in the seedling stage. Bulked segregant analysis (BSA) based on seedling tests was used to screen 418 SSR markers that covered the entire genome of wheat. Four markers, Xwmc453, Xcfd43, Xcfd77, and Xgwm484, were mapped within a chromosome region that spanned 9.7 cM from Sr6. The closest markers, Xwmc453 and Xcfd43, were linked to Sr6 at a distance of 1.1 and 1.5 cM, respectively. The markers Xwmc453 and Xcfd43 amplified Sr6-specific marker alleles that were diagnostic for Sr6 in a diverse set of 46 wheat accessions and breeding lines developed and/or collected in Australia, Canada, China, Egypt, Ethiopia, Kenya, Mexico, South Africa, and USA. These markers can now be used for marker-assisted selection of Sr6 and for pyramiding it with other stem rust resistance genes.     

Inheritance of resistance in water yam (Dioscorea alata) to anthracnose (Colletotrichum gloeosporioides)

Colletotrichum gloeosporioides causes anthracnose, the most severe foliar disease of field-grown water yam (Dioscorea alata). The inheritance of resistance to a moderately virulent (FGS) strain of the pathogen was investigated in crosses between tetraploid D. alata genotypes: TDa 95/00328 (resistant)×TDa 95–310 (susceptible) (cross A), and TDa 85/00257 (resistant)×TDa 92–2 (susceptible) (cross B). Segregation of F₁ progeny fitted genetic ratios of 3:1, 5:1 (crosses A and B) and 7:1 (cross A) resistant:susceptible when inoculated with the FGS strain, indicating that resistance is dominantly inherited and suggesting that more than one gene controls the inheritance of resistance to this strain in the accessions studied. When parental and progeny lines of cross A were inoculated with an aggressive (SGG) strain of the pathogen, all plants expressed a susceptible phenotype, indicating strain-specific resistance in TDa 95/00328. Screening of 20 cultivars/landraces confirmed the high susceptibility of D. alata accessions to the SGG strain and revealed the presence of apparent strain non-specific resistance in TDa 85/00257. TDa 85/00257 and TDa 87/01091 which were resistant to the SGG strain, will be useful both as sources of resistance and in the development of a host differential series for D. alata. Received: 15 May 2000 / Accepted: 18 October 2000     

A Thinopyrum ponticum and Triticum aestivum hybrid. Electrophoretic patterns of their endogenous phosphorylation, Diphosphonucleoside kinases, DNases and RNases

Endogenous protein phosphorylation, DNase and RNase electrophoretic patterns, and the detection of NDP-kinases by TLC (Thin Layer Chromatography) were performed in Thinopyrum ponticum (2n=10x=70), Triticum aestivum (2n=6x=42), and their hybrid seedlings in order to accomplish intergeneric hybridization. Octoploid intergeneric hybrids (2n=8x=56) were synthesized in less than 50% of the hybrids. The F₁ hybrid plants resembled Th. ponticum with regard to morphological features and were sterile. Hybrid seedlings revealed very low endogenous phosphorylation and very low NDP-kinase activity in comparison to their parents. In addition hybrid seedlings expressed a new nuclease. Received: 29 June 2000 / Accepted: 28 July 2000     

Complementary epistasis involving Sr12 explains adult plant resistance to stem rust in Thatcher wheat (Triticum aestivum L.)

Key message

Quantitative trait loci conferring adult plant resistance to Ug99 stem rust in Thatcher wheat display complementary gene action suggesting multiple quantitative trait loci are needed for effective resistance.

Abstract

Adult plant resistance (APR) in wheat (Triticum aestivum L.) to stem rust, caused by Puccinia graminis f. sp. tritici (Pgt), is desirable because this resistance can be Pgt race non-specific. Resistance derived from cultivar Thatcher can confer high levels of APR to the virulent Pgt race TTKSK (Ug99) when combined with stem rust resistance gene Sr57 (Lr34). To identify the loci conferring APR in Thatcher, we evaluated 160 RILs derived from Thatcher crossed to susceptible cultivar McNeal for field stem rust reaction in Kenya for two seasons and in St. Paul for one season. All RILs and parents were susceptible as seedlings to race TTKSK. However, adult plant stem rust severities in Kenya varied from 5 to 80 %. Composite interval mapping identified four quantitative trait loci (QTL). Three QTL were inherited from Thatcher and one, Sr57, was inherited from McNeal. The markers closest to the QTL peaks were used in an ANOVA to determine the additive and epistatic effects. A QTL on 3BS was detected in all three environments and explained 27–35 % of the variation. The peak of this QTL was at the same location as the Sr12 seedling resistance gene effective to race SCCSC. Epistatic interactions were significant between Sr12 and QTL on chromosome arms 1AL and 2BS. Though Sr12 cosegregated with the largest effect QTL, lines with Sr12 were not always resistant. The data suggest that Sr12 or a linked gene, though not effective to race TTKSK alone, confers APR when combined with other resistance loci.     

Inheritance of downy mildew resistance, β-1,3-glucanases and peroxidases in pearl millet [Pennisetum glaucum (L.) R. Br.] crosses

The inheritance of resistance to downy mildew disease and the defense-related enzymes β-1,3-glucanase and peroxidase was studied in crosses of pearl millet using a generation-mean analysis. The study material comprised six generations (susceptible and resistant parents, F₁, F₂, BC₁ and BC₂) in three crosses. Seedlings from these generations were inoculated with the downy mildew pathogen Sclerospora graminicola and disease incidence was recorded. Analysis of constitutive levels of β-1,3-glucanase and peroxidase in the seedlings of different generations indicated that the resistant populations showed higher enzyme activities, while lower activities of the enzymes were recorded in the susceptible populations. In the generation-mean analysis, the significance of scaling tests revealed the existence of non-allelic interactions in the inheritance of resistance to downy mildew as well as with the enzymes. Among the gene effects, both additive and dominant effects were significant. All the non-allelic interaction effects were significant in the crosses. Studies on the isozyme patterns of the enzymes substantiated the results of the disease-incidence experiments in most of the generations. The results indicated that the inheritance of downy mildew disease resistance and the expression of β-1,3-glucanase and peroxidase in pearl millet is not only under the control of additive and dominant genes but are also governed by complex non-allelic interactions. Received: 30 April 2000 / Accepted: 17 October 2000     

Normal Insulin Sensitivity in Lean Offspring of Obese Parents

Objective: Offspring of diabetic or hypertensive patients are insulin resistant at a prediabetic/prehypertensive stage. We tested the hypothesis that insulin action may be impaired in the offspring of obese nondiabetic parents. Research Methods and Procedures: Twenty‐one lean offspring of nonobese subjects [(OL) 22 ± 3 years of age] were matched to 23 lean offspring of obese subjects (OOb) by gender distribution, age, BMI, and waist circumference. Anthropometry, oral glucose tolerance, in vivo insulin sensitivity [by a euglycemic insulin clamp (6 pmol/min per kilogram_FFM; where FFM represents fat‐free mass)], and thermogenesis (by indirect calorimetry) were measured in each subject. The study subjects were from a population of 267 nuclear families (one offspring and both his/her parents) in which there was statistically significant (χ² = 30.2, p = 0.001) concordance of BMI between parents and offspring. Results: In comparing OOb with OL, no statistically significant difference or trend toward a difference was detected in fasting plasma glucose and insulin concentrations, glucose and insulin responses to oral glucose, insulin sensitivity [metabolism value = 45 ± 12 (OOb) vs. 47 ± 17 μmol/min per kilogram_FFM (OL)], insulin‐induced inhibition of protein and lipid oxidation, stimulation of glucose oxidation and nonoxidative glucose disposal, respiratory quotient, resting energy expenditure, and glucose‐induced thermogenesis. Discussion: The metabolic similarity between lean offspring of obese parents and those of nonobese parents suggests that insulin resistance and its correlates are not co‐inherited with the predisposition to develop obesity.     

Tagging and mapping of a rice gall midge resistance gene, <Emphasis Type="Italic">Gm8</Emphasis>, and development of SCARs for use in marker-aided selection and gene pyramiding

Using amplified fragment length polymorphisms (AFLPs) and random amplified polymorphic DNAs (RAPDs), we have tagged and mapped Gm8, a gene conferring resistance to the rice gall midge (Orseolia oryzae), a major insect pest of rice, onto rice chromosome 8. Using AFLPs, two fragments, AR257 and AS168, were identified that were linked to the resistant and susceptible phenotypes, respectively. Another resistant phenotype-specific marker, AP19₅₈₇, was also identified using RAPDs. SCAR primers based on the sequence of the fragments AR257 and AS168 failed to reveal polymorphism between the resistant and the susceptible parents. However, PCR using primers based on the regions flanking AR257 revealed polymorphism that was phenotype-specific. In contrast, PCR carried out using primers flanking the susceptible phenotype-associated fragment AS168 produced a monomorphic fragment. Restriction digestion of these monomorphic fragments revealed polymorphism between the susceptible and resistant parents. Nucleotide BLAST searches revealed that the three fragments show strong homology to rice PAC and BAC clones that formed a contig representing the short arm of chromosome 8. PCR amplification using the above-mentioned primers on a larger population, derived from a cross between two indica rice varieties, Jhitpiti (resistant parent) and TN1 (susceptible parent), showed that there is a tight linkage between the markers and the Gm8 locus. These markers, therefore, have potential for use in marker-aided selection and pyramiding of Gm8 along with other previously tagged gall midge resistance genes [Gm2, Gm4(t), and Gm7].The nucleotide sequence data reported here will appear in the EMBL, GenBank and DDBJ nucleotide sequence databases under the accession numbers AY545920–AY545923     

Inheritance of resistance to yellow rust (Phragmidium rubi-idaei) in red raspberry

The inheritance of resistance in red raspberry (Rubus idaeus) to yellow rust (Phragmidium rubi-idaei) was studied in a diallel cross among the cultivars Boyne, Meeker, Mailing Jewel, Glen Prosen and Glen Clova. The progenies and clonally propagated parents were exposed initially in a rust-infected plantation where the incidence and severity of infection was assessed at the telial stage. The following spring leaves on new canes of the same plants were inoculated with urediniospores in a glasshouse at 18 ± 2 °C. The latent period and number of uredinia per cm² of abaxial leaf surface were determined 13 and 18 days after inoculation. Cv. Boyne developed only chlorotic flecking on inoculated leaves in the glasshouse and no sporulation was observed. It is postulated that this reaction was determined by a major gene which is designated Yr. Some of the other parents showed incomplete resistance of the slow rusting type, and segregants of Boyne selfed that were susceptible also showed low levels of rust, which suggests that Boyne carries both major- and minor-gene resistance. Diallel analyses of both the field and glasshouse data from the susceptible segregates indicated that the degree of incomplete resistance present was determined predominantly by additive gene action, though small but significant non-additive effects also occurred: cv. Meeker was the most resistant parent and contributed the most resistance to the progenies. The Meeker progenies also segregated for gene H, which determines cane hairiness and is known to be associated with resistance to other diseases. Segregants without hairs (genotypes hh) were found to be the more resistant to rust.     

Ca ionophore-stimulated ion secretion in rabbit ileal mucosa: Relation to actions of cyclic 3′,5′-AMP and carbamylcholine

Summary Addition of the Ca ionophore, A23187 (0.5 g/ml) to the serosal side of stripped rabbit ileal mucosa, produced changes in ion transport qualitatively identical with those produced by cyclic 3,5-AMP (cAMP) and theophylline: an increase in short-circuit current and resistance, net secretion of Cl due both to a decrease in the unidirectional mucosa (m) to serosa (s) flux and an increase in the (s) to (m) flux, and net secretion of Na due to a decrease in (m) to (s) flux. Measurements of intracellular cAMP level demonstrated no change following incubation with the ionophore. Removal of Ca from the serosal bathing medium diminished the effects of A23187 but did not impair the action of theophylline. Furthermore, removal of Ca from both the mucosal and serosal bathing media by replacing it with Sr completely abolished the p.d. response to A23187. These results suggest that the ionophore elicits its secretory actions by increasing Ca influx into the epithelial cells. In a similar way, carbamylcholine and serotonin, secretagogues known to have no effect on intracellular cAMP level in intestinal mucosa, were shown to be dependent on extracellular Ca to produce their full electrical response (although, in the case of carbamylcholine at least, Sr can substitute for Ca). In contrast, the secretagogues vasoactive intestinal peptide and prostaglandin E₁, which raise cAMP concentration in intestinal mucosa, do not appear to require external Ca. It is interesting to speculate that Ca is an intracellular mediator of intestinal ion and water secretion and that some intestinal secretagogues may act as Ca ionophores.     

Genetic mapping of the stem rust (Puccinia graminis f. sp. tritici Eriks. & E. Henn) resistance gene Sr13 in wheat (Triticum aestivum L.)

Puccinia graminis f. sp. tritici, the causative agent of stem rust in wheat, is known for its high virulence variability and ability to evolve new virulence to resistance genes. Thus, pyramiding of several resistance genes in a single line is the best strategy for a sustainable control of wheat stem rust. Sr13 is one of the few resistance genes that are effective against wide ranging P. graminis f. sp. tritici races, including the pestilent race Ug99. Its effectiveness to Ug99 makes it a valuable source for resistance to stem rust. Molecular markers play a pivotal role in the genetic characterization of the new sources of resistance as well as in stacking two or more resistance genes in a single line. Therefore, the aim of this study was to develop molecular markers for Sr13 facilitating efficient pyramiding of Sr genes. Based on the 158 F₂ individuals derived from a cross of Khapstein/9*LMPG × Morocco and SSR analyses, the Sr13 locus was mapped on chromosome 6A of wheat, and a genetic map comprising about 90 cM was constructed with the closest marker barc37 being located 4.0 cM distally of Sr13. Of the nine mapped markers, barc37 amplified an allele specific for the presence of Sr13 as shown by testing different cultivars and breeding lines. These newly developed markers will increase the efficiency of incorporating Sr13 into cultivars that are widely adopted, but susceptible to hazardous Ug99 and/or assist for the development of new elite lines that are resistant to Ug99.