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Sudden death syndrome (SDS) of soybean is a complex of root rot disease caused by the semi-biotrophic fungus Fusarium solani f. sp. glycines (Fsg) and a leaf scorch disease caused by toxins produced by the pathogen in the roots. Development of partial rate-reducing resistance in roots to SDS was studied. The recombinant inbred line 23 (RIL23) that carried resistance conferred by six quantitative trait loci (QTL) derived from cultivars 'Essex' x 'Forrest' was compared to the susceptible cultivar Essex. Roots of RIL23 and its susceptible parent Essex were inoculated with Fsg. Transcript abundance (TA) of 191 ESTs was studied at five time points after inoculation. For most of the genes, there was an initial decrease in TA in the inoculated roots of both genotypes. By days 7 and 10 the inoculated roots of Essex failed to increase expression of the transcripts of defense-related genes. In RIL23 inoculated roots, the TA of 81 genes was increased by at least two-fold at day 3 (P=0.004), 88 genes at day 7 (P=0.0023) and 129 genes at day 10 (P=0.0026). A set of 35 genes maintained at least a two-fold higher abundance at all three time points. The increase in TA in RIL23 was in contrast to that observed in Essex where most of the ESTs showed either no change or a decreased TA. The ESTs with an increased TA had homology to the genes involved in resistance (analogs), signal transduction, plant defense, cell wall synthesis and transport of metabolites. Pathways that responded included the protein phosphorylation cascade, the phospholipase cascade and the phenolic natural products pathways, including isoflavone and cell wall synthesis.

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 x 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.

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Myo-inositol 1-phosphate synthase (MIPS; EC 5.5.1.4) converts glucose 6-phosphate to myo-inositol 1-phosphate in the presence of NAD+. It catalyzes the first step in the synthesis of myo-inositol and pinitol, and is a rate limiting step in the de novo biosynthesis of inositol in eukaryotes. Therefore, MIPS is involved in biotic and abiotic stress via Ca2+ signalling. Seedlings of four soybean genotypes were inoculated with Fusarium solani f. sp. glycines, the causative agent of sudden death syndrome (SDS), and differentially abundant mRNAs were identified by differential display. The genotypes carried either zero, two, four or six alleles of the quantitative trait loci (QTLs) that control resistance to SDS in an additive manner. The mRNA abundance of MIPS did not decrease following inoculation in a recombinant inbred line (RIL 23) containing all six resistance alleles of the QTLs conferring resistance to SDS of soybean. However, the abundance of MIPS mRNA was decreased in genotypes containing four, two or no resistance alleles. The specific activity of the MIPS enzyme in vitro followed the same pattern across genotypes. The IP3 content in the inoculated roots of genotypes with two, four or six resistance alleles were higher compared to the non-inoculated root. The results suggests that a non-additive effect on transcription and translation of MIPS is established in RIL 23 roots by pyramiding six QTLs for resistance to SDS. A role of MIPS in the partial resistance or response of soybean roots to F. solani infection is suggested. [ABSTRACT FROM AUTHOR]