Search

Abstract: The rhg1 gene or genes lie at a recessive or co-dominant locus, necessary for resistance to all Hg types of the soybean (Glycine max (L.) Merr.) cyst nematode (Heterodera glycines I.). The aim here was to identify nucleotide changes within a candidate gene found at the rhg1 locus that were capable of altering resistance to Hg types 0 (race 3). A 1.5 ± 0.25 cM region of chromosome 18 (linkage group G) was shown to encompass rhg1 using recombination events from four near isogenic line populations and nine DNA markers. The DNA markers anchored two bacterial artificial chromosome (BAC) clones 21d9 and 73p6. A single receptor like kinase (RLK; leucine rich repeat-transmembrane-protein kinase) candidate resistance gene was amplified from both BACs using redundant primers. The DNA sequence showed nine alleles of the RLK at Rhg1 in the soybean germplasm. Markers designed to detect alleles showed perfect association between allele 1 and resistance to soybean cyst nematode Hg types 0 in three segregating populations, fifteen additional selected recombination events and twenty-two Plant Introductions. A quantitative trait nucleotide in the RLK at rhg1 was inferred that alters A47 to V47 in the context of H297 rather than N297. Contiguous DNA sequence of 315 kbp of chromosome 18 (about 2 cM) contained additional gene candidates that may modulate resistance to other Hg-types including a variant laccase, a hydrogen-sodium ion antiport and two proteins of unknown function. A molecular basis for recessive and co-dominant resistance that involves interactions among paralagous disease-resistance genes was inferred that would improve methods for developing new nematode-resistant soybean cultivars.

Abstract: Expression of bacterial gdhA (glutamate dehydrogenase; GDH; E.C. 1.4.1.1) genes in transgenic plants fundamentally alters plant growth, herbicide tolerance and metabolite profiles. The aim was to correlate gdhA expression with water potential during deficit using transgenic Nicotiana tabacum cv. ‘SR1’ (tobacco). Expression of GDH activity from the transgene was significantly correlated with high water potentials during deficit, both after 5 days of water deprivation (R = 0.91) and after 6 h after re-watering on day 6 (R = 0.72). GDH expression may provide a tool to alter the response of plants to periodic water deficit.

Corn containing genetically engineered plasmid DNA encoding an Escherichia coliglutamate dehydrogenase (gdhA) was fed to 19-d-old weanling swine to trace the digestive fate of the transgenic DNA. Eight pens of 8 pigs were fed a commercial (nongdhA) starter for 2 wk. One pig was randomly selected from each pen for 0-h control samples. The remaining 56 pigs were transitioned onto a corn-soybean meal diet and fed a diet containing 58% gdhAcorn for approximately 1 wk; immediately thereafter, liver, 10th rib muscle, white blood cells, and plasma from the hepatic portal vein and ingesta from the stomach, distal ileum, and large intestine were collected. The DNA was extracted and the concentration determined via spectrophotometry. Polymerase chain reaction and gel electrophoresis were performed with primers designed to amplify 490 bp that included the plasmid's ligation site between the maize ubiquitin and the gdhAgenes. The gdhAcorn-derived DNA and diet served as positive assay controls, and conventional corn DNA and distilled water acted as negative assay controls. Detection limits were 0.99 fg of target DNA confounded with 500 ng of conventional corn DNA per each 20 &L reaction. Transgenic DNA was detected in 71.43% of the stomach and 1.79% of the ileal ingesta samples from treatment animals but was not detected in the large intestine, white blood cells, plasma, liver, or muscle samples. Transgenic DNA was not detected in any sample from 0-h control animals. Stomach and ileal ingesta samples were further analyzed using real-time PCR. With an estimated limit of detection of 1.049 ag/μL, 89.29% of the stomach ingesta samples were positive (average 1.56 fg target DNA). The proportion of transgenic DNA to total DNA differed between diet and stomach ingesta samples (P< 0.001). Despite the greater sensitivity of real-time PCR, target DNA was detected in only 1.79% of ileal ingesta. These data suggest that the gdhAtransgene began degradation in the stomach and was nondetectable in the large intestine.

With about 200 000 phytochemicals in existence, identifying those of biomedical significance is a mammoth task. In the postgenomic era, relating metabolite fingerprints, abundances, and profiles to genotype is also a large task. Ion analysis using Fourier transformed ion cyclotron resonance mass spectrometry (FT-ICR-MS) may provide a high-throughput approach to measure genotype dependency of the inferred metabolome if reproducible techniques can be established. Ion profile inferred metabolite fingerprints are coproducts. We used FT-ICR-MS-derived ion analysis to examine gdhA (glutamate dehydrogenase (GDH; EC 1.4.1.1)) transgenic Nicotiana tabacum (tobacco) carrying out altered glutamate, amino acid, and carbon metabolisms, that fundamentally alter plant productivity. Cause and effect between gdhA expression, glutamate metabolism, and plant phenotypes was analyzed by 13NH4+ labeling of amino acid fractions, and by FT-ICR-MS analysis of metabolites. The gdhA transgenic plants increased 13 N labeling of glutamate and glutamine significantly. FT-ICR-MS detected 2 012 ions reproducible in 2 to 4 ionization protocols. There were 283 ions in roots and 98 ions in leaves that appeared to significantly change abundance due to the measured GDH activity. About 58% percent of ions could not be used to infer a corresponding metabolite. From the 42% of ions that inferred known metabolites we found that certain amino acids, organic acids, and sugars increased and some fatty acids decreased. The transgene caused increased ammonium assimilation and detectable ion variation. Thirty-two compounds with biomedical significance were altered in abundance by GDH including 9 known carcinogens and 14 potential drugs. Therefore, the GDH transgene may lead to new uses for crops like tobacco.

Salmonellosis is a global problem caused by the international movement of foods and high incidence in exporting countries. In September 2001, in an outbreak investigation Australia isolated Salmonella Stanley from imported peanuts, which resulted in a wider investigation in Canada, England & Wales and Scotland. Patients infected with Salmonella serotypes known to be isolated from peanuts and reported to surveillance systems were interviewed to determine exposure histories. Tagged image file format (TIFF) images of pulsed-field gel electrophoresis (PFGE) patterns of Salmonella isolates were shared electronically amongst laboratories. Laboratories tested packets of ‘Brand X’ peanuts from various lots and product lines. In total, 97 cases of S. Stanley and 12 cases of S. Newport infection were found. Seventy-three per cent (71/97) of S. Stanley cases were in persons of Asian ethnicity. Twenty-eight per cent of cases recalled eating Brand X peanuts and a further 13% had peanuts in their house in the previous month or had eaten Asian-style peanuts. Laboratories isolated S. Stanley, S. Newport, S. Kottbus, S. Lexington and S. Unnamed from Brand X peanuts. Isolates of S. Stanley from peanuts and human patients were indistinguishable by PFGE. This international outbreak resulted from a product originating from one country affecting several others. Rapid sharing of electronic DNA images was a crucial factor in delineating the outbreak; multinational investigations would benefit from a harmonized approach.

Abstract. Soybean Sudden Death Syndrome (SDS) is caused by Fusarium solani f.sp. glycines (Fsg). Six quantitative trait loci (QTLs), each conferring partial resistance to SDS, have been discovered in an Essex × Forrest recombinant inbred line (RIL) population, but their mode of action is not clear. This study aimed to identify genes (ESTs) whose mRNA transcripts were altered in abundance in soybean roots following inoculation of Fsg. Roots of the soybean variety Forrest (four resistance alleles) were inoculated with Fsg, and 14 days later RNA sequences that were differentially expressed relative to uninoculated roots were enriched using suppression subtraction and differential display. The abundance of these RNAs was quantified in inoculated and non-inoculated roots by macroarray hybridizations. A unigene set of 135 ESTs was identified and used in a further macroarray analysis. The abundance of 28 cDNA fragments was increased more than two-fold in inoculated compared to uninoculated roots of RIL 23 (six resistance alleles). In Forrest and Essex (two resistance alleles), the level of only one mRNA was increased two-fold in inoculated roots compared to the uninoculated roots. In Essex most of the mRNAs analyzed decreased in abundance (61/135 showed a two-fold decrease), while in Forrest most mRNA abundances did not change. Among the 28 cDNAs that revealed a two-fold or higher increase in mRNA abundance in RIL 23, 14% code for proteins known to be involved in plant defense, 21% in metabolism, 14% in cell structure and 4% in transport. Unannotated ESTs accounted for 43% of the genes, and 4% of the sequences were previously unknown. The plant defense-related genes that showed a differential response to Fsg inoculation suggested a role for the phenylproponoid pathway in soybean defense against Fsg. In Essex, genes involved in plant defense, cell wall synthesis, ethylene synthesis and metabolism were expressed at lower levels in inoculated roots. The difference in response between the 2-, 4- and 6-gene pyramids suggests that QTLs for SDS resistance serve to delay symptoms or confer resistance by maintaining or increasing the expression of specific genes after inoculation/infection.

We investigated an outbreak of 54 cases of Salmonella Typhimurium phage type 9 (STM9) with a specific antibiotic resistance pattern. We used sequential analytic studies: two retrospective cohort studies, a case-control study, and a modified case-control study. An outbreak of salmonellosis due to Salmonella Typhimurium PT9 SSu (resistant to streptomycin and sulphafurazole) was identified. Fifty-four cases had illness onset from November 1998 to March 1999. Notifications commenced following a restaurant birthday party in December 1998. An initial cohort and case control study found no association with consumption of custard cake. However, case follow-up identified another cohort of people who had attended a birthday party in February at which 8/27 people who consumed a continental custard cake were ill compared to 0/10 who did not (P = 0.07). A revised case control study found illness was strongly associated with consumption of a particular continental custard cake (Mantel–Haenszel matched OR ∞, P = 0.00004). This report highlights the epidemiological value of using sequential study types, and persisting with the investigation of apparently sporadic food-borne outbreaks.

Some years ago, an increase in the number of sporadic cases and outbreaks of salmonellosis due to S. enterica serovar Bovismorbificans was observed in several European countries including Finland, Sweden, England/Wales, Austria, and Germany. In order to understand the recent spread of this serovar and to trace the route of infection back to its source, it was considered necessary to subtype S. Bovismorbificans isolates. Using phage typing (newly described here) and molecular fingerprinting (PFGE-pattern, plasmid profiles and ribotype) the isolates of European origin could be subtyped and compared to S. Bovismorbificans isolates that originated in overseas countries such as Australia, Thailand, India, etc. where this serovar was isolated more frequently. Significant clonal diversity was identified but some of the clonal types of S. Bovismorbificans dominated the epidemics and single cases in Europe as well as in overseas countries. The clonal identity among these isolates indicates an international distribution, new sources of infection, and highlights the urgent requirement for standardized laboratory based surveillance networks (e.g. Enter-Net). Moreover, it is suggested that strains of S. Bovismorbificans will continue to be of concern in public health and that phage typing together with PFGE typing can be applied as reliable and rapid tools for their future monitoring.

Molecular makers linked to quantitative trait loci (QTL) can assist soybean [Glycine max(L.) Merr.] breeders to combine traits of low heritability, such as yield, with disease resistance. The objective of this study was to identify markers linked to yield QTL in two recombinant inbred line (RIL) populations [‘Essex’ × ‘Forrest’ (E×F; n= 100) and ‘Flyer’ × ‘Hartwig’ (F×H; n= 94)] that also segregate for soybean cyst nematode (SCN) resistance genes (rhg1and Rhg4). Each population was yield tested in four environments between 1996 and 1999. The resistant parents produced lower yields. Heritability of yield across four environments was 47% for E×F and 57% for F×H. Yield was normally distributed in both populations. High yielding, SCN resistant transgressive segregants were not observed. In the E×F RIL population, 134 microsatellite markers were compared against yield by ANOVA and MAPMAKER QTL. Regions associated with yield were identified by SATT294 on linkage group (LG.) C1 (P= 0.006, R2= 10%), SATT440 on LG. I (P= 0.007, R2= 10%), and SATT337 on LG. K (P= 0.004, R2= 10%). Essex provided the beneficial allele at SATT337. Mean yields among F×H RILs were compared against 33 microsatellite markers from LG. K. In addition 136 markers from randomly selected LGs were compared with extreme phenotypes by bulk segregant analysis. Two regions on LG. K (20 cM apart) associated with yield were identified by SATT326 (P= 0.0004, R2= 15%) and SATT539 (P= 0.0008, R2= 14%). Flyer provided both beneficial alleles. Both populations revealed a yield QTL in the interval (5 cM) between SATT337 and SATT326. These populations may share a common allele for yield in this region, given that about 40% of Flyer genome derived from Essex.

Effective selection of field resistance to soybean sudden death syndrome (SDS) caused by Fusarium solani(Mart.) Sacc. f. sp. glycines(Fsg) (Roy, 1997), measured by disease index (DX), requires multiple environments. Current greenhouse assays reduce genotype × environment interactions, but fail to predict field resistance. Our objective was to compare selection for field resistance to SDS in the greenhouse among recombinant inbred lines (RILs) inoculated with Fsgat three rates. Thirty soybean [Glycine max(L.) Merr.] RILs with characterized field resistance to SDS were evaluated in the greenhouse for scorch severity at three inoculum rates in four experiments. Ten cultivars with characterized field resistance were compared using disease severity (DS) readings from one experiment at one inoculum rate. The heritability of DS among RILs in the greenhouse was 46% at the low, 66% at the moderate, and 37% at the high inoculum rates. Reduced inoculum rates in the greenhouse (3500 to 5000 spores cm−3plant growth medium) provided DS values that explained ≈65% of variation in the field Using a Fsginoculum rate of 5000 spores cm−3plant growth medium and greenhouse midparent DS as criterion for selection, the number of lines potentially resistant to SDS within a segregating population could be reduced by 53%. Errors caused ≈10% of field resistant lines to be eliminated. Among unrelated soybean cultivars, greenhouse DS values from an inoculum rate of 4000 spores cm−3plant growth medium explained 81 and 73% of variations in field DS and DX, respectively. Therefore, the method is an effective tool for inheritance studies and cultivar evaluation for SDS.

Soy products contain isoflavones (genistein, daidzein, and glycitein) that display biological effects when ingested by humans and animals, these effects are species, dose and age dependent. Therefore, the content and quality of isoflavones in soybeans is a key to their biological effect. Our objective was to identify loci that underlie isoflavone content in soybean seeds. The study involved 100 recombinant inbred lines (RIL) from the cross of ‘Essex’ by ‘Forrest,’ two cultivars that contrast for isoflavone content. Isoflavone content of seeds from each RIL was determined by high performance liquid chromatography (HPLC). The distribution of isoflavone content was continuous and unimodal. The heritability estimates on a line mean basis were 79% for daidzein, 22% for genistein, and 88% for glycitein. Isoflavone content of soybean seeds was compared against 150 polymorphic DNA markers in a one-way analysis of variance. Four genomic regions were found to be significantly associated with the isoflavone content of soybean seeds across both locations and years. Molecular linkage group B1 contained a major QTL underlying glycitein content (P=0.0001,R 2=50.2% ), linkage group N contained a QTL for glycitein (P=0.0033,R 2=11.1% ) and a QTL for daidzein (P=0.0023,R 2=10.3% ) and linkage group A1 contained a QTL for daidzein (P=0.0081,R 2=9.6% ). Selection for these chromosomal regions in a marker assisted selection program will allow for the manipulation of amounts and profiles of isoflavones (genistein, daidzein, and glycitein) content of soybean seeds. In addition, tightly linked markers can be used in map based cloning of genes associated with isoflavone content.

Abstract: In the soybean [Glycine max (L.) Merr.] cultivar ’Forrest’ a single chromosomal region underlies co-inheritance of field resistance of the sudden-death syndrome (SDS), caused by the fungus Fusarium solani (Mart.) Sacc. f. sp. glycines (Burk.) Snyd. & Hans. and soybean cyst nematode (SCN) race 3 (caused by Heterodera glycines Ichinohe). Our objectives were to verify that co-inheritance was derived from a single chromosomal region in near-isogenic lines and to separate component gene clusters. DNA markers were compared with a SDS leaf-scorch index (DX), F. solani root-infection severity (IS) and a SCN index of parasitism (IP) among 80 near-isogenic lines (NILs). The genomic region identified by the RFLP marker Bng122D was strongly associated (0.0004 ≤P≤ 0.006) with mean SDS DX (R 2 > 16–38%) and IS (R 2 > 38–73%), but only marginally associated with resistance to SCN. However, the linked (4.3–7.4 cM) microsatellite marker SATT309 was strongly associated with both resistance to SCN (0.0001 ≤P≤ 0.0003; R 2 > 24–97%) and mean leaf DX (0.0001 ≤P≤ 0.0003; R 2 > 25–63%), but not root IS. Recombination events among markers and traits enabled separation of the qualitative loci underlying resistance to SDS and SCN. Our data showed that resistance to SDS DX, SDS IS and SCN IP in Forrest may be caused by four genes in a cluster with two pairs in close linkage or by a two-gene cluster with each gene displaying pleiotropy, one conditioning SDS IS and DX and the other SCN IP and SDS DX.

DNA markers for genes conditioning resistance to soybean [Glycine max(L.) Merr.] root infection by [Fusarium solani(Mart.) Sacc. f. sp. glycine(Burk.)] (Rfs1), sudden death syndrome (SDS), and soybean cyst nematode (SCN; Heterodera glycinesIchinohe; Rhg4and rhg1) were previously identified in ‘Essex’ × ‘Forrest’. This study tests the effectiveness of those markers in selecting for disease resistance among recombinant inbred lines from ‘Flyer’ × ‘Hartwig’. A total of 535 among 739 lines were scored by two markers, providing four genotypes. A stratified random sample of 50 lines was evaluated for SDS by F. solaniroot infection severity at two locations and SCN race 3 index of parasitism in the greenhouse. Selection with BLT65 identified 281 among 671 lines with the genomic region that underlies Rhg4‐derived SCN resistance. Selection with Satt038 identified 230 among 613 lines containing the genomic region that underlies resistance to SDS (rfs1) and rhg1‐derived SCN resistance. A total of 93 out of 535 lines had genomic regions that underlie resistance to both SDS and SCN in Essex × Forrest. Segregation of both markers was not random (P≤ 0.05). Infection severity means for genotypes with the Hartwig allele at Satt038 (28–29%) were lower (P= 0.0001, R2= 28%) than with the Flyer allele (31–42%); irrespective of maturity group. BLT65 was not associated with infection severity. Mean SCN index of parasitism was lower (P≤ 0.05) only for genotypes carrying the Hartwig allele at both Satt038 and BLT65. Therefore, alleles conferring resistance to SDS and SCN in Essex × Forrest are transferable to other populations.

An automated early warning system has been developed and used for detecting clusters of human infection with enteric pathogens. The method used requires no specific disease modelling, and has the potential for extension to other epidemiological applications. A compound smoothing technique is used to determine baseline ‘normal’ incidence of disease from past data, and a warning threshold for current data is produced by combining a statistically determined increment from the baseline with a fixed minimum threshold. A retrospective study of salmonella infections over 3 years has been conducted. Over this period, the automated system achieved >90% sensitivity, with a positive predictive value consistently >50%, demonstrating the effectiveness of the combination of statistical and heuristic methods for cluster detection. We suggest that quantitative measurements are of considerable utility in evaluating the performance of such systems.

The unicellular cyanobacterium Synechococcus PCC6301 lacks a hybridisable homologue of the strongly conserved gdhA gene of E. coli that encodes NADP-specific glutamate dehydrogenase. This is consistent with the failure to find this enzyme in extracts of the cyanobacterium. The E. coli gdhA gene was transferred to Synechococcus PCC6301 by transformation with an integrative vector. High levels of glutamate dehydrogenase activity, similar to those found in ammonium grown E. coli cells, were found in these transformants. These transformed cyanobacteria displayed an ammonium tolerant phenotype, consistent with the action of their acquired glutamate dehydrogenase activity as an ammonium detoxification mechanism. Minor differences in colony size and in growth at low light intensity were also observed.

Severe losses of soybean [Glycine max(L.) Merr.] grain yield occur as a result of the disease sudden death syndrome (SDS), caused by Fusarium solani(Mart.) Sacc. f. sp. phaseoli(Burk.) Snyd. & Hans., type A. Selection for resistance to SDS is currently the most efficient means of yield protection. This study was undertaken within adapted soybean germplasm to identify and characterize loci underlying useful field resistance to SDS. One hundred eleven polymorphic DNA markers were compared with SDS disease response among 100 recombinant inbred lines derived from a cross between a durably SDS resistant cultivar, ‘Forrest’, and a SDS susceptible cultivar, ‘Essex’. SDS disease incidence (DI) and disease severity (DS) were determined in replicated, F. solaniinfested field‐test sites during 4 yr encompassing five locations. Four separate chromosomal segments were strongly associated with mean SDS DI across 5 locations (P< 0.001). In a previous report using the same genetic materials tested in the same environments two of these quantitative trait loci (QTL) had been identified. With the further analysis with 40 additional markers, two more QTL were detected. The two new QTL were stably associated with SDS resistance within each of five F. solaniinfested locations (P< 0.007). These two loci were identified by RAPD markers OI03450and OG13490and by OE04450and OE021000. The alleles that conferred resistance were both derived from Forrest. Jointly, the four QTL accounted for about 65% of total phenotypic variability in mean DI and 50% in mean DS. DNA markers can be used to define alleles conferring resistance to SDS. Selection for the SDS resistance QTL may allow efficient selection of resistant genotypes with good yield potential in F. solaniinfested fields.

One genomic region in soybean [Glycine max(L.) Merr.] ‘Essex’ and three in ‘Forrest’ underlie field resistance to sudden death syndrome (SDS) leaf scorch in their recombinant inbred line (RIL) progeny. Root infection by Fusarium solani(Mart.) Sacc. f. sp. glycineprecedes the leaf scorch caused by SDS. Forrest shows rate‐reducing resistance to both root colonization by F. solaniand leaf scorch, whereas Essex does not. Our objective was to determine whether genomic regions that underlie resistance to the SDS leaf scorch also caused resistance to root colonization by F. solaniin near‐isogeneic lines (NILs). The NILs were derived from individual plants selected from within one recombinant‐inbred line (ExF34). ExF34 was heterogenous within regions of linkage group C2 and G, each of which encompassed quantitative trait loci (QTL) for resistance to SDS. Using DNA markers, four genotypiclasses could be identified. The QTL effects were compared with two SDS disease parameters, leaf scorch measured as SDS disease index (DX) at the R6 growth stage and root colonization by F. solanimeasured as infection severity (IS) the R5.5 and R8 growth stages. The Forrest allele of the genomic region on linkage group G was consistently associated with decreased DX (P< 0.05–0.0004) and IS (P< 0.05–0.0017). The Essex allele the genomic region on linkage group C2 caused a decrease in DX (P> 0.05) and IS in the susceptible pair of the four NIL clases R5.5 but not R8. Therefore, the QTL on linkage group G and C2 confer separate components of resistance to SDS that are suitable for selection in a resistance gene pyramid.

Restriction fragment length polymorphism (RFLP) was determined among P. vulgaris genotypes and Phaseolus species using 19 probes. The incidence of polymorphism was high (70–86%) between species, but relatively low (22–26%) between genotypes of P. vulgaris. Suitable probes were identified for the analysis of P. vulgaris and P. coccineus hybrids. The segregation pattern in F2 populations was Mendelian for two probes (LHB and VEE20) and non-Mendelian for GS-g, CHS, and CHI. Statistical analyses indicated gametic selection with preferential transmission of the P. vulgaris alleles, which may account for the selective recovery of P. vulgaris progeny types observed earlier. The available hybrids of P. vulgaris and P. coccineus and the high degree of interspecific RFLP will facilitate the construction of a linkage map for Phaseolus.

DNA probes from the narG gene of Escherichia coli, which encodes the large polypeptide of respiratory nitrate reductase, show cross-hybridization at low stringency to a single region of the genome of the cyanobacterium Synechococcus PCC6301. This segment of cyanobacterial DNA was cloned as the insert of plasmid pDN1 and characterized. RNA complementary to pDN1 was shown to be substantially more abundant in nitrate grown cells of Synechococcus PCC6301 than in ammonium grown cells, thus parallelling the nitrate induction and ammonium repression of nitrate reductase activity in cultures of this cyanobacterium. A mutant of Synechococcus PCC6301 deficient in nitrate reductase activity was obtained after a potentially mutagenic transformation treatment using pDN1 as a donor. This mutant was restored to the wild type phenotype following stable integrative transformation with pDN1 DNA. Taken together these data suggest that pDN1 might encode a polypeptide of nitrate reductase. pDN1 is distinct from three clones of genes involved in nitrate assimilation that were isolated previously from the related cyanobacterium Synechococcus PCC7942 (Kuhlemeier et al., 1984a, J.Bact. 159, 36–41, and 1984b, Gene 31, 109–116).

Coinheritance of field resistance of soybean [Glycine max(L.) Merr.] to sudden death syndrome (SDS) [caused by the fungus Fusarium solani(Mart.) Sacc. f. sp. phaseoli(Burk.) Snyd. & Hans.] and soybean cyst nematode (SCN) race 3 (caused by Heterodera glycinesIchinohe) sometimes occurs in crosses among adapted cultivars. Our objective was to characterize the loci underlying this coinheritance. One hundred thirty DNA markers were compared with SDS disease response and SCN score among 100 recombinant inbred lines (RILs) derived from a cross between SDS and SCN resistant ‘Forrest’ and SDS and SCN susceptible ‘Essex’. SDS disease incidence (DI) was determined in replicated sites during 4 yr encompassing five locations. The SCN score was determined in the greenhouse from naturally infested field soil samples. Two separate genomic regions identified by random amplified polymorphic DNA (RAPD) markers OI03450and OW15400were associated with mean SCN score (P= 0.0001) and jointly accounted for about 47% of variability in SCN score. OI03450identified a QTL for resistance to SCN (R2= 14%) within a genomic region that was strongly associated with SDS DI (R2= 20%), partly explaining the coinheritance of the two traits. This locus could be assigned to the region of linkage group G already known to encompass the major SCN resistance locus.

Yield losses occur in soybean [Glycine max(L.) Merr.] because of sudden death syndrome (SDS) caused by Fusarium solani(Mart.) Saec. f. sp. phaseoli(Burk.) Snyd. & Hans, type A. Our objective was to determine whether tolerance or partial resistance to infection underlies field resistance to SDS. Seven field resistant cultivars and five susceptible cultivars were planted at two locations. Twenty taproots per cultivar were sampled every 7 to 21 d from the V0 to R8 growth stages, 8 to 121 days after planting (DAP). Six taproot sections per plant were tested for F. solanion a selective medium. Infection frequency (IF), the percentage of infected plants, and infection severity (IS), the percentage of infected root segments, were scored. Leaf symptoms were recorded and standardized to the R6 stage and the disease index (DX) was calculated. Infection was detected at the VI stage (within 15 DAP) and reached a maximum by about R1 (55–68 DAP). All cultivars were infected by F. solani. However, seasonal mean IF and mean IS were significantly lower among the resistant cultivar class. After R1, infection was also significantly lower among the resistant cultivar class within individual sampling dates. Also, DX and IF were correlated in each environment (r= 0.38 and 0.61). Therefore, in the resistant cultivars Forrest, Ripley, Jack, PI520733, ExF44, ExF59, and ExF78, late season rate‐reducing (partial) resistance decreased the DX, IF, and IS. Resistance probably extends the latent period of F. solani. Among susceptible cultivars, Essex and A5403, had reduced leaf symptoms but high IF and IS suggesting tolerance to F.solanithat alleviated SDS.

Explains how archaeologists use remote-sensing technology, such as color-infrared photography (CIR), heat-detecting infrared scanners, and ground-penetrating radar to locate ruins and other ancient features. Anasazi Indian sites in Colorado and New Mexico; Galisteo Basin, New Mexico; Thermal infrared-multi-spectral scanner (TIMS); Work by anthropologist Frank W. Eddy of the University of Colorado.

Soybean seeds contain large amounts of isoflavones or phytoestrogens such as genistein, daidzein, and glycitein that display biological effects when ingested by humans and animals. In seeds, the total amount, and amount of each type, of isoflavone varies by 5 fold between cultivars and locations. Isoflavone content and quality are one key to the biological effects of soy foods, dietary supplements, and nutraceuticals. Previously we had identified 6 loci (QTL) controlling isoflavone content using 150 DNA markers. This study aimed to identify and delimit loci underlying heritable variation in isoflavone content with additional DNA markers. We used a recombinant inbred line (RIL) population (n=100) derived from the cross of “Essex” by “Forrest,” two cultivars that contrast for isoflavone content. Seed isoflavone content of each RIL was determined by HPLC and compared against 240 polymorphic microsatellite markers by one-way analysis of variance. Two QTL that underlie seed isoflavone content were newly discovered. The additional markers confirmed and refined the positions of the six QTL already reported. The first new region anchored by the marker BARC-Satt063 was significantly associated with genistein (P=0.009, R2=29.5%) and daidzein (P=0.007, R2=17.0%). The region is located on linkage group B2 and derived the beneficial allele from Essex. The second new region defined by the marker BARC-Satt129 was significantly associated with total glycitein (P=0.0005, R2=32.0%). The region is located on linkage group D1a+Q and also derived the beneficial allele from Essex. Jointly the eight loci can explain the heritable variation in isoflavone content. The loci may be used to stabilize seed isoflavone content by selection and to isolate the underlying genes.

A 6-week-old child with acute urinary tract infection caused by Shiga toxin—producing Escherichia coli (STEC) O5:H—developed hemolytic-uremic syndrome (HUS). Molecular and phenotypic analysis of the urinary isolate indicated that it lacked uropathic properties and that it was probably of intestinal origin. Nevertheless, the patient did not experience a diarrheal prodrome, nor was STEC or Shiga toxin detected in his feces at any time. Examination of the patient's serum pointed to recent infection with E. coli O5, with no evidence of exposure to E. coli O157, O111, or O26. A review of 13 previously reported cases of HUS associated with acute urinary tract infection indicated that this was the first case of nondiarrheal HUS in which infection with the most common STEC serogroups was specifically excluded. This case illustrates the need to investigate patients with nondiarrheal HUS for infection with STEC.