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 (QTN) [corrected] in the RLK at rhg1 was inferred that alters A87 to V87 in the context of H274 rather than N274. [corrected] 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.

Candidate genes were identified for two loci, QRfs2 providing resistance to the leaf scorch called soybean (Glycine max (L.) Merr.) sudden death syndrome (SDS) and QRfs1 providing resistance to root infection by the causal pathogen Fusarium solani f.sp. glycines. The 7.5 +/- 0.5 cM region of chromosome 18 (linkage group G) was shown to encompass a cluster of resistance loci using recombination events from 4 near-isogenic line populations and 9 DNA markers. The DNA markers anchored 9 physical map contigs (7 are shown on the soybean Gbrowse, 2 are unpublished), 45 BAC end sequences (41 in Gbrowse), and contiguous DNA sequences of 315, 127, and 110 kbp. Gene density was high at 1 gene per 7 kbp only around the already sequenced regions. Three to 4 gene-rich islands were inferred to be distributed across the entire 7.5 cM or 3.5 Mbp showing that genes are clustered in the soybean genome. Candidate resistance genes were identified and a molecular basis for interactions among the disease resistance genes in the cluster inferred.

To obtain more information on the Hevea brasiliensis genome, we sequenced the transcriptome from the vegetative shoot apex yielding 2 311 497 reads. Clustering and assembly of the reads produced a total of 113 313 unique sequences, comprising 28 387 isotigs and 84 926 singletons. Also, 17 819 expressed sequence tag (EST)-simple sequence repeats (SSRs) were identified from the data set. To demonstrate the use of this EST resource for marker development, primers were designed for 430 of the EST-SSRs. Three hundred and twenty-three primer pairs were amplifiable in H. brasiliensis clones. Polymorphic information content values of selected 47 SSRs among 20 H. brasiliensis clones ranged from 0.13 to 0.71, with an average of 0.51. A dendrogram of genetic similarities between the 20 H. brasiliensis clones using these 47 EST-SSRs suggested two distinct groups that correlated well with clone pedigree. These novel EST-SSRs together with the published SSRs were used for the construction of an integrated parental linkage map of H. brasiliensis based on 81 lines of an F1 mapping population. The map consisted of 97 loci, consisting of 37 novel EST-SSRs and 60 published SSRs, distributed on 23 linkage groups and covered 842.9 cM with a mean interval of 11.9 cM and ∼4 loci per linkage group. Although the numbers of linkage groups exceed the haploid number (18), but with several common markers between homologous linkage groups with the previous map indicated that the F1 map in this study is appropriate for further study in marker-assisted selection.

ments over several years which is expensive, time consuming, and labor intensive (Maughan et al., 1996). Molecular makers linked to quantitative trait loci (QTL) can assistComponents of yield are often identifiable which aid soybean [Glycine max (L.) Merr.] breeders to combine traits of low heritability, such as yield, with disease resistance. The objective of this the selection of yield (Fehr, 1987;Specht et al., 1999). study was to identify markers linked to yield QTL in two recombinantIn soybeans, the basis of yield improvement is unclear, inbred line (RIL) populations ['Essex' ϫ 'Forrest' (EϫF; n ϭ 100) but maturity and growth habit have major effects (Manand 'Flyer' ϫ 'Hartwig' (FϫH; n ϭ 94)] that also segregate for soybean sur et al., 1996;Orf et al., 1999;Specht et al., 1999). cyst nematode (SCN) resistance genes (rhg1 and Rhg4 ). Each popula-Resistance to disease is usually a strong component of tion was yield tested in four environments between 1996 and 1999. yield in disease infested environments (Njiti et al., 1998). The resistant parents produced lower yields. Heritability of yield Disease resistance in cultivars (particularly SCN resisacross four environments was 47% for EϫF and 57% for FϫH. Yield tance) has consistently been associated with a 1-2% was normally distributed in both populations. High yielding, SCN decrease in yield when disease was absent (Concibido resistant transgressive segregants were not observed. In the EϫF RIL et al., 1997). In addition, many SCN resistant cultivars population, 134 microsatellite markers were compared against yield by ANOVA and MAPMAKER QTL. Regions associated with yield appear to display poor combining ability during interwere identified by SATT294 on linkage group (LG.) C1 (P ϭ 0.006, crossing (Concibido et al., 1997). Sudden death syn-R 2 ϭ 10%), SATT440 on LG. I (P ϭ 0.007, R 2 ϭ 10%), and SATT337 drome (SDS) resistance has also been associated with on LG. K (P ϭ 0.004, R 2 ϭ 10%). Essex provided the beneficial allele low yield potential (Rupe et al., 1993). at SATT337. Mean yields among FϫH RILs were compared against Genetic maps have been useful for soybean genome 33 microsatellite markers from LG. K. In addition 136 markers from analysis. Maps have allowed the identification of many randomly selected LGs were compared with extreme phenotypes by economically important soybean genes conditioning bulk segregant analysis. Two regions on LG. K (20 cM apart) associquantitative trait loci (QTL), including those for disease ated with yield were identified by SATT326 (P ϭ 0.0004, R 2 ϭ 15%)