1. Plant Nutrients. 2. The Soil as a Plant Nutrient Medium. 3. Nutrient Uptake and Assimilation. 4. Plant Water Relationships. 5. Plant Growth and Crop Production. 6. Fertilizer Application. 7. Nitrogen. 8. Sulphur. 9. Phosphorus. 10. Potassium. 11. Calcium. 12. Magnesium. 13. Iron. 14. Manganese. 15. Zinc. 16. Copper. 17. Molybdenum. 18. Boron. 19. Further Elements of Importance. 20. Elements with More Toxic Effects. General Readings. References. Index.

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Principles of plant nutrition

PATHWAY OF ETHYLENE BIOSyNTHESIS 156 Methionine as an Intermediate ....... 157 S-Adenosylmethionine as an Intermediate 158 I-Aminocyclopropanecarboxylic Acid as an Intermediate . ......... 158 Methionine Cycle ........ 161 Conversion of l-Aminocyclopropanecarboxylic Acid to Ethylene 164 REGULATION OF ETHYLENE BIOSYNTHESIS 167 Regulation in Ripening Fruits and Senescing Flowers ...... 167 Auxin-Induced Ethylene Production 169 Regulation of Ethylene Biosynthesis by Ethylene 169 Stress-Induced Ethylene Production . . . . . . . . 171 Regulation by Light and Carbon Dioxide 173 Inhibitors of Ethylene Biosynthesis : 174 Conjugation of l-Aminocyclopropanecarboxylic Acid to l-(Malonylamino) cyclopropanecarboxylic Acid 178 CONCLUDING REMARKS 180

Ethylene biosynthesis and its regulation in higher plants

Seed dormancy is an innate seed property that defines the environmental conditions in which the seed is able to germinate. It is determined by genetics with a substantial environmental influence which is mediated, at least in part, by the plant hormones abscisic acid and gibberellins. Not only is the dormancy status influenced by the seed maturation environment, it is also continuously changing with time following shedding in a manner determined by the ambient environment. As dormancy is present throughout the higher plants in all major climatic regions, adaptation has resulted in divergent responses to the environment. Through this adaptation, germination is timed to avoid unfavourable weather for subsequent plant establishment and reproductive growth. In this review, we present an integrated view of the evolution, molecular genetics, physiology, biochemistry, ecology and modelling of seed dormancy mechanisms and their control of germination. We argue that adaptation has taken place on a theme rather than via fundamentally different paths and identify similarities underlying the extensive diversity in the dormancy response to the environment that controls germination.

/pdf/seed-dormancy-and-the-control-of-germination-4tdhm2985s.pdf

Seed dormancy and the control of germination

The variation in growth rate with temperature of unicellular algae suggests that an equation can be written to describe the maximum expected growth rate for temperatures less than 40°C. Measured rates of phytoplankton growth in the sea and in lakes are reviewed and compared with maximum expected rates. The assimilation number (i.e., rate of photosynthetic carbon assimilation per weight of chlorophyll a) for phytoplankton photosynthesis is related to the growth rate and the carbon/chlorophyll a ratio in the phytoplankton. Since maximum expected growth rate can be estimated from tempera­ ture, the maximum expected assimilation number can also be estimated if the carbon/ chlorophyll a ratio in the phytoplankton crop is known. Many investigations of phytoplankton photosynthesis in the ocean have included measures of the assimilation number, while fewer data are available on growth rate. Assimilation numbers for Antarctic seas are low as would be expected from the low ambient temperatures. Tropical seas and temperate waters in summer often show low assimilation numbers as a result of low ambient nutrient concentrations. However, coastal estuaries with rapid nutrient regeneration processes show seasonal variations in the assimilation number with temperature which agree well with expectation. The variation in maximum expected growth rate with temperature seems a logical starting point for modeling phytoplankton growth and photosynthesis in the sea.

Temperature and phytoplankton growth in the sea

Auxin: regulation, action, and interaction.

The paper deals with the general problem of the physiological basis of branching, and the roles of known and unexplored factors in sensitivity to apical domirnance. It is shown that when pea seedling shoots are completely or partially inhibited by other shoots on the same plant auxin can promote their elongation, even though it does not have this effect on inhibited buds. This influence of auxin is only exerted on internodal elongation and not on apical growth. When kinetin in a solution of alcohol and carbowax is applied directly to the lateral buds of pea seedlings, it releases them from inhibition by the growing apex. It is shown that the role of alcohol in this solution is to act as a surfactant, permitting good contact with the buds, while that of carbowax, being hygroscopic, is to maintain a thin film of solution over the buds. Buds thus released from apical dominance by kinetin do not elongate as much as do uninhibited control buds. Such kinetintreated buds can, however, be made to elongate normally by the application of auxin locally to their apices. It is concluded that growing shoots are relatively insensitive to correlative inhibition because they synthesize two types of growth substances, namely, auxin, which antagonizes the inhibitory effect on internodal elongation, and cytokinins, which permit the apex itself to develop. In the discussion it is brought out that many cases of branching, which appear at first to bear little relation to one another, can be understood on the basis of two principles, namely: (1) Any reduction in the growth rate of a dominant apex reduces its inhibitory effect on other apices, and (2) once an apex starts growing it becomes less sensitive to inhibition by other apices These generalizations and the experimental results are tentatively interpreted in terms of an interaction between the syntheses of auxin and of cytokinin.

The role of auxins and cytokinins in the release of buds from dominance

The Antagonism of Auxin and Kinetin in Apical Dominance

On the nature of inhibitions caused by auxin.

IT has been shown with isolated stem sections bearing a single bud that the development of this bud can be inhibited by indolyl-3-acetic acid (IAA) or other auxins, and this inhibition released by kinetin1. The concentrations of IAA needed are physiological, and the whole phenomenon appears identical with that of normal apical dominance. Nevertheless, the question remains as to whether the same release can be obtained in the intact plant, that is, under conditions of apical dominance sensu stricto.

Release of Lateral Buds from Apical Dominance

By growth experiments in indoleacetic acid-1-(14)C (IAA), and determination of the (14)CO(2) evolved, it has been shown directly that polyphenols synergize IAA-induced growth by counteracting IAA decarboxylation. Sinapic and ferulic acids act like polyphenols. Endogenous polyphenols doubtless exert the same influence in intact plants. Monophenols stimulate the decarboxylation of IAA under conditions where they depress growth. When Mn(++) is present as well, this effect is enhanced. All these growth effects are paralleled by effects on the isolated IAA oxidizing enzyme of Avena.EDTA acts like the polyphenols in depressing the decarboxylation of IAA, and not synergizing with the growth induced by naphthalene-acetic acid (NAA) and 2,4-D. However, since EDTA synergizes with IAA for growth even at optimal IAA concentrations, its growth promotion probably involves an additional effect.DIECA inhibits powerfully the destruction of IAA, but without causing much growth promotion, apparently because its decomposition products inhibit respiration.Mn(++) alone stimulates the decarboxylation of IAA, i.e. this ion promotes the IAA oxidase in vivo as it does in vitro. Nevertheless, it does not inhibit elongation, but at relatively high concentrations even stimulates it, both at low and high IAA levels. Since Mn(++) also promotes the growth induced by NAA and 2,4-D, its growth action cannot rest primarily on modifying the metabolism of the auxins.Cobalt somewhat decreases the decarboxylation of IAA, but this cannot explain its growth promotion, since Co(++), like Mn(++), stimulates elongation even at optimal IAA concentrations, and acts with NAA just as well as with IAA. Ferrous ion, on the other hand, acts like the polyphenols.Floating pea stem sections exude enough organic matter to support bacteria which after 7 hours cause considerable decarboxylation of IAA. Avena coleoptile sections have a comparable though smaller effect after 12 hours.The present experiments, with those of others, point to a major role for polyphenolase in controlling hormone balance, since the introduction into a phenolic molecule of a second, adjacent hydroxyl group changes the action from auxin-destroying to auxin-preserving. Thus the phenol oxidizing enzymes must act as general growth controllers.

Kenneth V. Thimann

Papers

The role of auxins and cytokinins in the release of buds from dominance

The Antagonism of Auxin and Kinetin in Apical Dominance

On the nature of inhibitions caused by auxin.

Release of Lateral Buds from Apical Dominance

Interactions of phenolic acids, metallic ions and chelating agents on auxin-induced growth.