Plant dormancy has a major impact on the cultivation of plants, influencing such processes as seed germination, flowering, and vegetative growth. The diversity of plant tissues that exhibit, or contribute to the manifestation of, dormancy is great, and there appear to be numerous mechanisms of dormancy induction or release. This complexity was discussed by Romberger (55) nearly 25 years ago. Yet his analysis of the unresolved challenges in dormancy research is still valid today, for the overall understanding of dormancy is limited. This lack of understanding may be due, in part, to the abundance of terminology that has arisen without a nomenclatural framework in which to classify and relate the events being described.

Experiments with olive (Olea europaea L.) shoot explants were carried out to determine the influence of winter chilling on the release of axillary buds from dormancy. This investigation was designed to explore an alternative explanation for the confusing concept surrounding the role of chilling in olive floral induction. Leafy explants collected from 10 Nov. to 6 Mar. were grown in a greenhouse under mist at 13/24C (night/day) and in a growth chamber at 10/21C (night/day) to determine the end of dormancy. Growth of floral buds from leafy explants was first recorded from 5 Jan. samples. After that date the percentage of developing floral buds and rate of their development increased. Floral bud abscission, increase in bud fresh weight, and simultaneous decrease of relative bud dry weight were associated with growth initiation of floral buds. Manual defoliation of adult trees during the period of shoot explant collection indicated that leaves play a critical role in development once the floral buds had completed dormancy. Supplementary chilling of isolated shoots collected 20 Jan. demonstrated that 7.2C was sufficient to complete chilling requirements, while 12.5C allowed both the completion of chilling requirements and the proper temperature for subsequent floral bud growth. Winter chilling is required to release previously initiated floral buds from dormancy, and we question the previous concept that the role of chilling is to induce olive floral initiation.

GA3 scaffold injections applied between May and November to nonbearing olive (Olea europea L.) trees inhibited flowering the following year, increased shoot width when applied in May, June, and July, and increased inflorescence length when applied in November and February. Fruit removal and seed destruction were effective in improving the return bloom in `Manzanillo' olives when done before endocarp sclerification. Depending on-the year, endocarp sclerification takes place 7 to 8 weeks after full bloom (AFB), usually about 1 July. Fruit removal had no effect on flowering when done after this time. Scaffold injection of paclobutrazol applied to bearing trees between May and September did not affect flowering the following year. The results of our research supports the hypothesis that olive flower induction occurs around the time of endocarp sclerification. Chemical names used: gibberellic acid (GA3), (2RS,3RS)-1-(4-chlorophenyl)-4-dimethyl-2-1,2-4-triazol-1-yl) pentan-3-ol(paclobutrazol).

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Natural enemies have long been used in biological control programs to mitigate the damage caused by herbivory. Many herbivorous insect species also act as plant virus vectors, enabling virus transmission from plant to plant and hence disease development in a plant population. Whilst an intuitive assumption would be to expect a decrease in vector numbers to lead to subsequent reductions in virus transmission, recent evidence suggests that introduction of natural enemies (parasitoids and predators) may in some cases increase plant virus transmission while at the same time reducing vector numbers. In this paper we review the evidence for plant-virusvector-natural enemy interactions, the signalling mechanisms involved and their implications for virus transmission, and show how a modelling approach can assist in identifying the key parameters and relationships involved in determining the disease outcome. A mathematical model linking the population dynamics of a vector-parasitoid system with virus transmission was used to investigate the effects of virus inoculation and acquisition rates, parasitoid attack rate and vector aggregation on disease dynamics across a wide range of parameter value combinations. Virus spread was found to increase with enhanced inoculation, acquisition and parasitoid attack rate but decrease with high levels of vector aggregation.