Separate loci underlie resistance to root infection and leaf scorch during soybean sudden death syndrome

Soybean [Glycine max (L.) Merr.] cultivars show differences in their resistance to both the leaf scorch and root rot of sudden death syndrome (SDS). The syndrome is caused by root colonization by Fusarium virguliforme (ex. F. solani f. sp. glycines). Root susceptibility combined with reduced leaf scorch resistance has been associated with resistance to Heterodera glycines HG Type 1.3.6.7 (race 14) of the soybean cyst nematode (SCN). In contrast, the rhg1 locus underlying resistance to Hg Type 0 was found clustered with three loci for resistance to SDS leaf scorch and one for root infection. The aims of this study were to compare the inheritance of resistance to leaf scorch and root infection in a population that segregated for resistance to SCN and to identify the underlying quantitative trait loci (QTL). “Hartwig”, a cultivar partially resistant to SDS leaf scorch, F. virguliforme root infection and SCN HG Type 1.3.6.7 was crossed with the partially susceptible cultivar “Flyer”. Ninety-two F5-derived recombinant inbred lines and 144 markers were used for map development. Four QTL found in earlier studies were confirmed. One contributed resistance to leaf scorch on linkage group (LG) C2 (Satt277; P = 0.004, R 2 = 15%). Two on LG G underlay root infection at R8 (Satt038; P = 0.0001 R 2 = 28.1%; Satt115; P = 0.003, R 2 = 12.9%). The marker Satt038 was linked to rhg1 underlying resistance to SCN Hg Type 0. The fourth QTL was on LG D2 underlying resistance to root infection at R6 (Satt574; P = 0.001, R 2 = 10%). That QTL was in an interval previously associated with resistance to both SDS leaf scorch and SCN Hg Type 1.3.6.7. The QTL showed repulsion linkage with resistance to SCN that may explain the relative susceptibility to SDS of some SCN resistant cultivars. One additional QTL was discovered on LG G underlying resistance to SDS leaf scorch measured by disease index (Satt130; P = 0.003, R 2 = 13%). The loci and markers will provide tagged alleles with which to improve the breeding of cultivars combining resistances to SDS leaf scorch, root infection and SCN HG Type 1.3.6.7

Definition of Soybean Genomic Regions That Control Seed Phytoestrogen Amounts

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 ([Formula: see text]) 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 ([Formula: see text] , [Formula: see text]) and daidzein ([Formula: see text] , [Formula: see text]). 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 ([Formula: see text] , [Formula: see text]). 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

Genomic regions that underlie soybean seed isoflavone content

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)fr om the cross of ‘Essex’ by ‘Forrest,’ two cultivars that contrast for isoflavone content. Isoflavone content of seeds fromeach 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,R2 = 50.2%), linkage group N contained a QTL for glycitein (P = 0.0033,R2 = 11.1%)and a QTL for daidzein (P = 0.0023,R2 = 10.3%) and linkage group A1 contained a QTL for daidzein (P = 0.0081,R2 = 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)c ontent of soybean seeds. In addition, tightly linked markers can be used in map based cloning of genes associated with isoflavone content

‘Forrest’ Resistance to the Soybean Cyst Nematode Is Bigenic: Saturation Mapping of the Rhg1 and Rhg4 Loci

Field resistance to cyst nematode (SCN) race 3 (Heterodera glycines I.) in soybean [Glycine max (L.) Merr.] cv ‘Forrest’ is conditioned by two QTLs: the underlying genes are presumed to include Rhg1 on linkage group G and Rhg4 on linkage group A2. A population of recombinant inbred lines (RILs) and two populations of near-isogenic lines (NILs) derived from a cross of Forrest × Essex were used to map the loci affecting resistance to SCN. Bulked segregant analysis, with 512 AFLP primer combinations and microsatellite markers, produced a high-density genetic map for the intervals carrying Rhg1 and Rhg4. The two QTLs involved in resistance to SCN were strongly associated with the AFLP marker EATGMCGA87 (P = 0.0001, R2 = 24.5%) on linkage group G, and the AFLP marker ECCGMAAC405 (P = 0.0001, R2 = 26.2%) on linkage group A2. Two-way analysis of variance showed epistasic interaction (P = 0.0001, R2 =16%) between the two loci controlling SCN resistance in Essex × Forrest recombinant inbred lines. Considering the two loci as qualitative genes and the resistance as female index FI \u3c 5%, jointly the two loci explained over 98% of the resistance. The locations of the two QTLs were confirmed in the NILs populations. Therefore SCN resistance in Forrest × Essex is bigenic. High-efficiency marker-assisted selection can be performed using the markers to develop cultivars with stable resistance to SCN

Loci underlying resistance to manganese toxicity mapped in a soybean recombinant inbred line population of Essex

Abstract Resistance to manganese toxicity is associated with some soybean (Glycine max) cultivars grown on acidic soils or in hydroponics. Previously random amplified polymorphic DNA (RAPD) markers had seemed to identify 4 quantitative trait loci (QTL), regions that might underlie resistance to manganese toxicity in a recombinant inbred line (RIL) population derived from 'Essex' x 'Forrest'. Our objective was to identify microsatellite markers linked to these, or additional, QTL for resistance to manganese toxicity in a separate assay. Two hundred and forty microsatellite markers and 100 RILs were used to construct a map. The response of five plants per genotype to manganese was measured by leaf chlorosis (scored from 0-5) and root necrosis (scored from 0-5) from 7-28 days after treatment with 125 µM of manganese in hydroponics. The experiment was repeated. ANOVA and MapMaker/QTL were used to identify regions underlying the responses. Three genomic regions on different linkage groups were found to contain QTL for resistance to necrosis during manganese toxicity. The regions located on linkage groups C2 (BARC_Satt291), I (BARC_Satt239) and G (OP_OEO2) were each significantly associated (P < 0.005, R 2 = 20%) with root necrosis at 7 days after treatment. The regions all derived the beneficial allele from Essex. One of the previously identified RAPD associated root necrosis QTL was identified in this new study. However, no QTL for leaf chlorosis were detected (P < 0.005) and none of the RAPD identified leaf chlorosis QTL could be identified. We conclude that root and leaf resistance to manganese toxicity are environmentally sensitive quantitative traits determined by separate loci of different number and magnitude of effect