Biological Control of Protomycopsis phaseoli, the Causal Agent of Leaf Smut of Cowpea

Among the bacteria and fungi associated from the soil where cowpea was grown and tested for antagonism against Protomycopsis phaseoli , Bacillus sp. inhibited the radial growth, Fusarium oxysporum , yeast, Aspergillus fumigatus , Trichoderma harzianum , Trichoderma koningii and Trichoderma sp. reduced radial growth of P. phaseoli . In vitro studies showed that T. harzianum was an active hyperparasite and more effective in reducing the radial growth of P. phaseoli than T. koningii and Trichoderma sp. Spore suspensions of the three Trichoderma spp. prevented the germination of chlamydospores of P. phaseoli . In the field, when applied as spray, Trichoderma sp. was found to be more active in reducing the spread of leaf smut disease than T. harzianum and T. koningii.     

Stimulation and inhibition of myoblast differentiation by hormones

Summary The growth and differentiation of L6 myoblasts are subject to control by two proteins secreted by cells of the Buffalo rat liver line. The first of these, rat insulinlike growth factor-II (formerly designated multiplication stimulating activity) is a potent stimulator of myoblast proliferation and differentiation, as well as associated processes such as amino acid uptake and incroporation into protein, RNA synthesis, and thymidine incorporation into DNA. In addition, this hormone causes a significant decrease in the rate of protein degradation. All of these actions seem to be attributable to a single molecular species, although their time courses and sensitivity to the hormone differ substantially. The second protein, the differentiation inhibitor (DI), is a nonmitogenic inhibitor of all tested aspects of myoblast differentiation, including fusion and the elevation of creatine kinase. Indirect immunofluorescence experiments demonstrated that DI also blocks accumulation of myosin heavy chain and myomesin. Upon removal of DI after 72 h incubation, all of these effects were reversed and normal myotubes containing the usual complement of muscle-specific proteins were formed. Thus, this system makes it possible to achieve specific stimulation or inhibition of muscle cell differentiation by addition of purified proteins to cloned cells in serum-free medium. This work was supported by a Muscular Dystrophy Association Postdoctoral Fellowship (M. J. E.-H.), U.S. Public Health Service Grant HL-11551 and AG-00629 (J. R. F.) and AM-28433 (B. M. V.), and a grant from the Muscular Dystrophy Association (J. R. F.).     

Stimulation by glucocorticoids of myoblast growth at low cell densities

Proliferation of rat myoblasts was stimulated by addition of 10(-7) M dexamethasone to cells plated at 25 cells/cm(2). In the presence of fetal calf serum and chick embryo extract, physiological levels of glucocorticoids caused a 3- to 7-fold increase in colony formation. In mass cultures, proliferation of myoblasts was also stimulated by dexamethasone, but fibroblast growth was inhibited. These opposite effects of glucocorticoids on myoblast and fibroblast growth suggest their use in cloning muscle cells from mixed cell populations.