During soybean seed germination, the expansive growth potential of the embryonic axes is driven by water uptake while cell wall loosening occurs in cells from the elongation zone (EZ). Expansins are regarded as primary promoters of cell wall remodelling in all plant expansion processes, with the expression profiles of the soybean expansins supporting their cell or tissue specificity. Therefore, we used embryonic axes isolated from whole seed and focused on the EZ to study seed germination. Using a suite of degenerate primers, we amplified an abundantly expressed expansin gene at the EZ during soybean embryonic axis germination, which was identified as EXP1 by in silico analyses. Expression studies showed that EXP1 was induced under germination conditions in distilled water and down-regulated by abscisic acid (ABA), which inhibits soybean germination by physiologically restraining expansion. Moreover, we also identified a time window of ABA responsiveness within the first 6 h of incubation in water, after which ABA lost control of both EXP1 expression and embryonic axis germination, thus confirming the early role of EXP1 in the EZ during this process. By contrast, EXP1 levels in the EZ increased even when germination was impaired by osmotically limiting the water availability required to develop the embryonic axes’ growth potential. We propose that these higher EXP1 levels are involved in the fast germination of soybean embryonic axes as soon as water availability is re-established. Taken together, our results show strong EXP1 expression in the EZ and postulate EXP1 as a target candidate for soybean seed germination control.

The germination of developing seeds is very uncommon and is generally associated with deficiencies in abscisic acid (ABA) synthesis or sensitivity. This paper examines the quantitative relationship between the inhibition of precocious germination and endogenous ABA in the embryonic axis (ABAa) of hydrated soybean [Glycine max (L.) Merr.] seeds, isolated after the completion of histodifferentiation and before the beginning of dehydration, as well as the magnitude and evolution of axis sensitivity to endogenous ABA during that period. Developing seeds harvested at 25, 30, 35, 40 and 45 d after anthesis (DAA) were subjected to incubation or washing to induce changes in ABA content. ABA content was measured by radioimmunoassay, using a monoclonal antibody against free ABA. Germinability was measured as the time to 50% germination (t 50 ). Washing and incubation induced eight-and twofold increases, respectively, in the rate of ABAa decline compared with the in planta ABAa decline. The threshold ABAa for inhibition of precocious germination (ABAc) increased slightly from 25 to 40 DAA [1.15 -1.66 mg ABA (g DW) 21 ]. This contrasted with the substantial decline in ABAa [10.90 -2.07 mg ABA (g DW) 21 ] during the same period, and indicated that sensitivity to endogenous ABA of hydrated seeds was initially high and diminished slowly during development. The relationship between (ABAa -ABAc) and t 50 was linear for immature seeds incubated before and after washing. Below the ABAc, there were no differences in the t 50 of 25 -45 DAA seeds. The ABAa contribution to the control of precocious soybean seed germination was evident, although other potentially interacting factors were also present.

The first report of soybean stem canker (SSC) caused by Diaporthe phaseolorum var. caulivora in South America was published in 2001, and was based on an isolate obtained in 1999 at Oliveros, Santa Fe (32°33′S, 60°51′W), Argentina (2). During the 2001 to 2002 growing season, isolates of D. phaseolorum var. caulivora were obtained from stems of field-grown soybeans (Glycine max L.) exhibiting SSC symptoms. Isolates were collected in three localities of the main soybean-producing region of Argentina: Marcos Juárez, Córdoba (32°66′S, 62°10′W); Salto, Buenos Aires (34°20′S, 60°33′W); and Diego de Alvear, Santa Fe (34°21′S, 62°10′W), and disease incidence in the fields was 10 to 60%, 5 to 15%, and 10 to 20%, respectively. The pathogen was isolated on potato glucose agar acidified with 0.2% lactic acid cultured in the dark at 25 ± 1°C. White colonies with compact and tufted mycelium were produced and turned yellow and light tan after 6 days. Appressed and fluffy mycelia were observed in old cultures. Stromata (2 mm diameter) were produced but pycnidia were not detected. After 20 days in culture at 25 ± 1°C under a 12-h light and 12-h dark regime, clustered perithecia developed on stem segments. For each isolate, 10 perithecia, 90 asci, and 30 bicellular, biguttulate ascospores were measured. Averages of asci length and width were 28.3 ± 2.3 and 5.9 ± 0.7 μm, respectively. Averages of ascospores mean length and width were 8.4 ± 0.6 and 2.5 ± 0.4 μm, respectively. These measures were similar to the measures obtained previously (2). Based on these features, the new isolates were classified as D. phaseolorum var. caulivora (Athow & Caldwell). Clustered perithecia, smaller asci and ascospores, and the development of fluffy mycelia with age were the main characteristics that distinguished D. phaseolorum var. caulivora from D. phaseolorum var. meridionalis (1). Pathogenicity trials were performed on cvs. Tracy M, Crockett, Hutchenson, and RA 702 in the greenhouse by placing a small amount of mycelium in soybean seedling hypocotyls wounds made with a scalpel. The pathogen was reisolated from stem portions of the symptomatic plants. Control plants remained healthy. The results reported here show that D. phaseolorum var. caulivora is widely disseminated in the main soybean-producing region of Argentina, where it coexists with D. phaseolorum var. meridionalis (2). The coexistence of both varieties indicates pathogen variability in the region is higher than previously recognized. References: (1) R. N. Pioli et al. Plant Dis. 83:1071, 1999. (2) R. N. Pioli et al. Plant Dis. 85:95, 2001.

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