Gibberellin was first discovered in Japan, prior to World War II, by scientists who were studying rice infected with the "foolish-seedling" disease. The causal agent is a fungus that triggers plants to grow taller than normal and eventually lodge. The name of the family of gibberellin compounds was taken from the fungus. Nearly 100
endogenous compounds have been found in plants that contain gibberellin-like activity. To simplify gibberellin notation, they are listed as GAn.
Over the years, we have recognized that most of the gibberellins identified in plants are precursors or degradation products that occur in the biosynthesis and metabolism of this hormone. Since different plant families possess different pathways of gibberellin synthesis and degradation, not all gibberellins are present in a given species. In fruit crops, the gibberellins of import are GA3, GA4, and GA7. These appear to be present endogenously in plant and fruit tissues and can also be applied exogenously as plant growth regulators. For more information on gibberellin chemistry and endogenous changes that occur during fruit development, see Westwood (1993).
In fruit plants, gibberellins are synthesized primarily in young, expanding leaves just below the meristem, in developing seeds, and in rapidly growing fruit tissues. Unlike auxin, gibberellin can be translocated in any direction throughout the plant. Gibberellins play three developmental roles in fruit plants, corresponding to their sites of synthesis. In vegetative tissues, gibberellins play a major role in cell expansion that occurs just below the apical meristem. They stimulate cell expansion in the rapidly growing area below the meristem. As such, they are associated with internode length, and hence vegetative vigor. Since excessive vegetative growth is not desirable, gibberellin synthesis inhibitors such as paclobutrazol and uniconazole are of interest in fruit production. In fruit development, two events are regulated by gibberellin levels in the tissue: (1) the suppression of flower bud initiation in pome fruit by seed-produced gibberellins and (2) cell expansion during "final swell" of fruit with a double-sigmoid growth pattern, such as stone fruit.
Biennial bearing was a problem that vexed apple growers for centuries. Until the discovery of plant hormones, it was assumed that biennial bearing was required for nutritional reasons, so the tree could replenish reserves lost in cropping. M. A. Blake's classic experiments in hand thinning demonstrated that flower bud initiation is de-velopmentally regulated in apple. If fruit are not removed early in the season, flowering is suppressed in the subsequent season. Chan and Cain (1967) demonstrated that the seeds are the source of the vegetative signal to the spur. Through exogenous applications, gibberellins were implicated as the hormone responsible for that vegetative signal.
In developing fleshy fruit with a final swell, gibberellins play a major role in determining final fruit size just prior to harvest. At that time, there is a dramatic increase in cell expansion and fresh weight gain in the fruit flesh. This correlates with increasing gibberellin responsiveness in the tissues.
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