Since the discovery of the plant growth-regulating properties of TRIA, a primary alcohol that is a natural constituent of plant waxes, and its second messenger L(+)-adenosine, the rapid response kinetics to these compounds have been enigmatic (Ries and Wert, 1988;Ries, 1991).TRIA increased the dry weight, free amino acids, reducing sugars, and soluble protein of rice (Oryza sativa L.) and maize (Zea mays L.) plants within 5 min (Ries, 1991). TRIA also elicited the appearance of L(+)-adenosine in the roots of plants whose shoots were sprayed with nanomolar concentrations within 1 min (Ries and Wert, 1988). This was the first evidence that L(+)-adenosine occurred in nature. Synthetic L(+)-adenosine increased the rate of growth of rice seedlings, as measured by total dry weight gain, by more than 50% within 24 h of foliar application of 0.01 to 100.0 kg L-' (3.7 X 10-" to 10-7 M), whereas D(-)-adenosine did not affect plant growth (Ries, 1991). 49site plant part, providing it was applied 1 min prior to TRIA application (Ries and Wert, 1988). TRIA applied to oat (Avena sativa L.) or tomato (Lycopersicon esculentum Mill.) shoots connected to rice roots by a 4-mm water column also resulted in the appearance of L(+)-adenosine (TRIM) in rice roots (Ries and Wert, 1988).In an attempt to determine other physiological responses to TRIA in addition to the elicitation of L(+)-adenosine, 20-to 25-d-old tomato seedlings were sprayed with water or TRIA, and after 1 min the plants were excised. Analysis of the diffusate from the excised shoots, as determined by HPLC and atomic absorption spectrophotometry, indicated large concentration differences in organic compounds and inorganic cations (unpublished data). The largest differences were in the cation concentration of the exudate from the stump of the excised tomato plant. Thus, the objective of this research was to use this observation to further elucidate the mode of action for the rapid responses of plants to TRIA and L(+)-adenosine.We present here evidence that foliar applications of both of these compounds at nanomolar concentrations cause rapid changes in soluble Ca2+, Mg2+, and K+ concentrations within xylem exudates from the stumps of excised stems and leaves. MATERIALS A N D METHODS Plant Crowth and TreatmentTomatoes (Lycopersicon esculentum Mill. cv Sunny), cucumbers (Cucumis sativa L. cv Flurry), and maize (Zea mays L.cv Pioneer 3780) were grown in a greenhouse with approximately 16 h of supplemental light (700 pmol s-' m-', metal halide) daily. Seeds were planted in 15-cm diameter clay pots containing a soil mix, and the plants were thinned to two or three per pot 8 to 10 d after emergence. Soluble fertilizer (20 N-8.6 P-16.6 K; 1.0 g L-' Peters 20-20-20, W.R. Grace and Co., Fogelsville, PA) was applied once or twice after planting and again prior to treatment. The pots were labeled, randomized for treatments within blocks, and isolated from each other on the greenhouse bench. They were not disturbed for several hours prior to initiation of the treatments.Experiment...

To investigate the role of Ca(2+)-independent forms of protein kinase C (PKC) in ischemic neuronal injury, mRNA expression of PKC was studied by Northern blot analysis. Ischemia was produced in gerbils by 10-min bilateral carotid artery occlusion and was followed by recirculation for 15 min, 6 h, and 24 h. Brains of postischemic and sham-operated animals were removed, forebrains fresh frozen, and processed for Northern blot analysis. Three synthetic oligonucleotide probes based on published cDNA sequences of rat brain PKC for the isozymes delta, epsilon, and zeta were utilized for hybridization. Northern blot analysis showed increased hybridization signal for all three PKC isozymes examined in the 6- and 24-h postischemic groups. Of these, the twofold increases in the expression of PKC delta and zeta were statistically significant in comparison to the control. These results suggest that the mRNA levels of Ca(2+)-independent forms of PKC, in particular, delta and zeta, are temporally stimulated by ischemic injury in the brain and may imply an important role of the enzyme in postischemic neuronal damage. However, since the protein itself was not examined in this study, the significance of the increased expression cannot be ascertained. However, it may reflect a compensatory response to the loss of PKC reported to occur in the reperfusion phase.

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The activity of malate dehydrogenase (MDH, EC 1.1.1.37) in rice (Oryza sativa L. cv. California M‐201) roots was increased within 25 min by a foliar application of 37 nM of 9‐β‐l(+)‐adenosine [l(+)‐adenosine]. A similar concentration of 9‐β‐d(‐)‐adenosine [d(‐)‐adenosine] did not affect MDH. Triacontanol (2.7 nM) which elicits l(+)‐adenosine in plants also increased MDH activity in roots of rice seedlings. whereas neither octacosanol nor a mixture of equimolar concentrations of triacontanol and octacosanol had any effect on MDH activity. l(+)‐Adenosine increased MDH activity of rice seedlings grown at 10.20 and 40°C. The effect was measurable 24 h after application at 10 and 20°C, but not 6 h after treatment at 40°C. Ninety minutes after l(+)‐adenosine was applied to the foliage of plants grown at 10, 20 and 40°C, MDH activity in the roots was 40, 30 and 9% more, respectively, than in the untreated controls. The concentration of water soluble protein was also increased by l(+)‐adenosine and was positively correlated with MDH activity. When measured 90 min after application of l(+)‐adenosine at different times of day, MDH activity and dry weight were increased most when l(+)‐adenosine was applied 9 and 12 h after the lights came on in a 16‐h photoperiod. The optimum light intensity for the response of rice to l(+)‐adenosine, as measured by MDH activity, was 450 μmol m−2 s−1.