Molecular mapping of five soybean genes involved in male-sterility, female-sterility.

In soybean, asynaptic and desynaptic mutants lead to abnormal meiosis and fertility reduction. Several male-sterile, female-sterile mutants have been identified and studied in soybean, however, some of these mutants have not been mapped to locations on soybean chromosomes. The objectives of this study were to molecularly map five male-sterile, female-sterile genes (st2, st4, st5, st6, and st7) in soybean and compare the map locations of these genes with already mapped sterility genes. Microsatellite markers were used in bulked segregant analyses to locate all five male-sterile, female-sterile genes to soybean chromosomes, and markers from the corresponding chromosomes were used on F2 populations to generate genetic linkage maps. The st2, st4, st5, st6, and st7 genes were located on molecular linkage group (MLG) B1 (chromosome 11), MLG D1a (chromosome 01), MLG F (chromosome 13), MLG B2 (chromosome 14), and D1b (chromosome 02), respectively. The st2, st4, st5, st6, and st7 genes were flanked to 10.3 (∼ 399 kb), 6.3 (∼ 164 kb), 3.9 (∼ 11.8 Mb), 11.0 (∼ 409 kb), and 5.3 cM (∼ 224 kb), and the flanked regions contained 57, 17, 362, 52, and 17 predicted genes, respectively. Future characterization of candidate genes should facilitate identification of the male- and female-fertility genes, which may provide vital insights on structure and function of genes involved in the reproductive pathway in soybean.

Aged lymphocyte proliferation following incorporation and retention of dietary omega-3 fatty acids.

T cell activation involves events at the plasma membrane; therefore, molecules such as long chain omega-3 fatty acids that alter the structure of the plasma membrane may affect the activation of aged T cells. In this project we investigated whether the incorporation of omega-3 fatty acids (from fish oil), in the presence of vitamin E, improves age-diminished T cell proliferation. Young and old mice were fed diets rich in either fish (menhaden) oil or saturated fat for various lengths of time. Splenocytes were harvested from these mice and stimulated in culture with either mitogen or the antigen keyhole limpet hemocyanin (for a secondary response); proliferation was estimated by [3H]thymidine incorporation. We found no discernible effect of dietary omega-3 fatty acids (with vitamin E supplementation) on lymphocyte proliferation stimulated by the mitogens concanavalin A or phytohemagglutinin. We did, however, find that the saturated fat diet and the menhaden oil diet in young mice lowered protein kinase C activities in the particulate fractions of spleen cells when compared to chow-fed mice. Middle-aged and old mice were less affected by the experimental diets than young mice, but they demonstrated decreased protein kinase C activity as well. These alterations did not affect the ability of splenocytes to respond to mitogenic stimulation. Fatty acid analysis revealed that lymphocytes from mice fed saturated fat for 8.5 months retained significant amounts of the omega-3 fatty acid docosahexaenoic acid, despite the lack of dietary omega-3 fatty acids. However, when aged (but not young) lymphocytes were clonally expanded by antigen in vivo in the presence of dietary omega-3 fatty acids, they produced a greater secondary proliferative response than old lymphocytes expanded during a saturated fat diet. Although our results suggest that omega-3 fatty acids may enhance aged lymphocyte proliferation, the tenacious retention of these fatty acids makes comparison with omega-3-depleted lymphocytes difficult.