Physiological Changes in Phaseolus vulgaris in Response to Long-term Ozone Exposure

The effects of ozone on Phaseolus vulgaris cv. Lit were investigatedusing open-top chambers (OTCs) ventilated with charcoal andPurafil filtered air (CF treatments), ambient air (NF treatments)and ambient air to which low, medium or high concentrationsof ozone were added (NFL, NFM and NFH). Ozone additions of 8,16 and 23 nl l^–1 were made during phase 1 of the experiment(0–44 d after emergence, DAE), and additions of 15, 30and 47 nl l^–1 were made during phase 2 (45–99 DAE).Ozone was added to the chambers between 1100 and 1800 h GMT,for 3 or 4 consecutive days each week. The seasonal 7-h meanozone concentrations were 8, 21, 27, 33 and 38 nl l^–1in the CF, NF, NFL, NFM and NFH treatments, respectively. No visible symptoms of ozone injury or significant physiologicalchanges were detected in P. vulgaris during phase I of the experiment.In phase 2, the photosynthesis (Pn) and stomatal conductance(gs) of NFH-plants were inhibited by 73% and 86%, respectively,during ozone exposure, and recovered to pre-exposure valueson the following day. These observations were made prior tothe appearance, 60 DAE, of bronze lesions on the leaves of NFH-plants.The photosynthetic capacity and gs of NFH-leaves decreased asthe severity of ozone injury increased. Rates of weight lossfrom excised leaves also increased with increasing ozone injury.Microscopic investigations of the bronzed regions revealed extensivecellular breakdown, including tonoplast and chloroplast enveloperupture, and the aggregation of the cytoplasmic contents towardsone end of the cell. Severely damaged leaves abscised from the plants, resultingin premature canopy senescence in the NFM and NFH treatments.This, coupled with the lower photosynthetic capacity of existingleaves led to 25 % lower yield in the NFH than the NF treatment(P < 0.05). Phaseolus vulgaris, green bean, ozone, symptom development, photosynthesis, cell ultrastructure     

The detection of apple chlorotic leafspot virus by a modified procedure of enzyme-linked immunosorbent assay (ELISA)

The technique of enzyme-linked immunosorbent assay (ELISA) was modified to enable detection of apple chlorotic leafspot virus (CLSV) both in herbaceous hosts and in several naturally infected fruiting and ornamental woody host species. Some of the characteristics of the modified method as used with different virus-host combinations are described.     

Adelphamoeba galeacystis n. g., n. sp., an Amoeboflagellate Isolated from Soil*

SYNOPSIS. An amoeboflagellate isolated from common soil is described. The amoeboid stage is typically limax and contains a well differentiated uroid region. The flagellate has 2 flagella, which emerge anteriorly and are equal in length. It has a ventral cytostome near the anterior border. The cyst is helmet-shaped and without opercula. Polar masses are present during nuclear division.     

Protein Kinase C and Melanocyte Transformation

Melanoma cells which have been isolated from metastatic melanoma tissue are able to survive and proliferate in serum supplemented media. In contrast, normal human melanocytes require the presence of growth stimulators if they are to survive in culture. A tumor promotor, 12–0-tetradecanoyl-phorbol-13-acetate (TPA) and substances that increase intracellular levels of cyclic-adenosine-monophosphate (cAMP), such as cholera toxin or isobutylmethyl xanthine, have been widely used for this purpose. The phorbol diester receptor was shown in 1982 to be the phospholipid- and calcium-dependent enzyme protein kinase C (PKC). We therefore directed our studies to the role of PKC regulation in the growth of normal human melanocytes and their transformation. Our studies show that while melanoma cells are inhibited by TPA, the growth of normal melanocytes is stimulated in a dose-dependent manner. The inhibitor, 1-(5-isoquinolinesulfonyl)-2-methyl-piperizine dihydrochloride (H7), which has been found to be the most specific for PKC, had no effect on the growth of normal melanocytes, but inhibited the growth of melanoma cells in a dose-dependent manner. PKC was isolated from the membrane and cytosol of normal melanocytes and melanoma cells. The basal (resting) levels of PKC activity in normal melanocytes was low compared to that measured in melanoma cells, and after short-term (1 hour) treatment with TPA the PKC activity was greatest at the membrane, with the activity decreasing the cytosol. Upon prolonged (48 hours) treatment with TPA, this redistribution of activity continued in normal melanocytes and the total activity increased. In melanoma cells, however, the total PKC activity decreased, particularly in the membrane fraction. A difference in activity and distribution of the enzyme was also seen after short-term (1 hour) treatment with H7. There was very little effect seen on PKC in normal melanocytes; however, the effect on melanoma cells was similar to that seen after 48 hours of exposure to TPA with a decrease in total activity, particularly in the membrane fraction. These results indicate that the regulation of PKC, in particular its activation by TPA, is altered during the transformation of normal human melanocytes     

Recognition of Bacterial Initiator tRNA by an Initiation Factor

Initiation factor F2a of E. coli seems to recognize only fMet-tRNA_f. This may be analogous to the recognition of other aminoacyl-tRNAs by elongation factor T.     

Development of Eimeria auburnensis in Cell Cultures

SYNOPSIS. Monolayer established cell line cultures of bovine kidney (Madin-Darby) and human intestine (Intestine 407), as well as embryonic bovine tracheal and embryonic spleen cell line cultures were inoculated with E. auburnensis sporozoites and observed for a maximum of 22 days. Mature 1st generation schizonts developed in the kidney, tracheal and spleen cells. In the intestine cells, trophozoites were seen in 3 of 4 experiments, but schizonts were not found. Sporozoites penetrated cells, beginning within a few minutes after inoculation. Penetration was usually accomplished within 10 seconds, and the body of the sporozoite underwent a slight constriction as it passed thru the host cell membrane. Some sporozoites left cells. Numerous intracellular sporozoites were observed in kidney, tracheal and spleen cultures. Crescent bodies were seen in the parasitophorous vacuole as early as 1 day after inoculation. At this time, the nuclei of most intracellular sporozoites had changed from vesicular to compact. Beginning 4 days after inoculation, enlarged sporozoites and parasites having a sporozoite shape, but with 2-5 nuclei, were frequently seen. These enlarged sporozoites and sporozoite-shaped schizonts evidently transformed into trophozoites and spheroidal schizonts by means of lateral outpocketings. Few trophozoites were seen. More immature schizonts developed in kidney cells than in the other cell types. The numbers of mature schizonts observed in kidney and tracheal cells were similar, but development occurred less consistently in the latter. Few immature and mature schizonts developed in spleen cells. Mature schizonts, first seen 9 days after inoculation, were considerably smaller than those reported from calves. Some motile merozoites were seen; evidently no development beyond these occurred. The nucleus and nucleolus of host cells were enlarged; this enlargement was not as pronounced as in infections in calves. Multiple host cell nuclei were frequently observed. Degenerative changes in the cultured cells and in the parasites usually occurred, beginning 9-17 days after inoculation; these were more pronounced in the spleen cells than in the others.