Gibberellins (GAs) are plant hormones that regulate growth and influence various developmental processes, including stem elongation, germination, dormancy, flowering, sex expression, enzyme induction, and leaf and fruit senescence.[1]
Gibberellin was first recognized in 1926 by a Japanese scientist, Eiichi Kurosawa, studying bakanae, the "foolish seedling" disease in rice.[1][2] It was first isolated in 1935 by Teijiro Yabuta and Sumuki, from fungal strains (Gibberella fujikuroi) provided by Kurosawa.[1] Yabuta named the isolate as gibberellin.[1]
Interest in gibberellins outside of Japan began after World War II. In the United States, the first research was undertaken by a unit at Camp Detrick in Maryland, via studying seedlings of the bean Vicia faba.[1] In the United Kingdom, work on isolating new types of gibberellin was undertaken at Imperial Chemical Industries.[1] Interest in gibberellins spread around the world as the potential for its use on various commercially important plants became more obvious. For example, research that started at the University of California, Davis in the mid-1960s led to its commercial use on Thompson seedless table grapes throughout California by 1962.[3] A known antagonist to gibberellin is paclobutrazol (PBZ), which in turn inhibits growth and induces early fruitset as well as seedset.
All known gibberellins are diterpenoid acids that are synthesized by the terpenoid pathway in plastids and then modified in the endoplasmic reticulum and cytosol until they reach their biologically-active form.[4] All gibberellins are derived via the ent-gibberellane skeleton, but are synthesised via ent-kaurene. The gibberellins are named GA1 through GAn in order of discovery. Gibberellic acid, which was the first gibberellin to be structurally characterized, is GA3.
As of 2003, there were 126 GAs identified from plants, fungi, and bacteria.[1]
Gibberellins are tetracyclic diterpene acids. There are two classes based on the presence of either 19 or 20 carbons. The 19-carbon gibberellins, such as gibberellic acid, have lost carbon 20 and, in place, possess a five-member lactone bridge that links carbons 4 and 10. The 19-carbon forms are, in general, the biologically active forms of gibberellins. Hydroxylation also has a great effect on the biological activity of the gibberellin. In general, the most biologically active compounds are dihydroxylated gibberellins, which possess hydroxyl groups on both carbon 3 and carbon 13. Gibberellic acid is a dihydroxylated gibberellin.[5]
Gibberellins are involved in the natural process of breaking dormancy and various other aspects of germination. Before the photosynthetic apparatus develops sufficiently in the early stages of germination, the stored energy reserves of starch nourish the seedling. Usually in germination, the breakdown of starch to glucose in the endosperm begins shortly after the seed is exposed to water.[6] Gibberellins in the seed embryo are believed to signal starch hydrolysis through inducing the synthesis of the enzyme α-amylase in the aleurone cells. In the model for gibberellin-induced production of α-amylase, it is demonstrated that gibberellins (denoted by GA) produced in the scutellum diffuse to the aleurone cells, where they stimulate the secretion α-amylase.[4] α-Amylase then hydrolyses starch, which is abundant in many seeds, into glucose that can be used in cellular respiration to produce energy for the seed embryo. Studies of this process have indicated gibberellins cause higher levels of transcription of the gene coding for the α-amylase enzyme, to stimulate the synthesis of α-amylase.[5]
Gibberellins are produced in greater mass when the plant is exposed to cold temperatures. They stimulate cell elongation, breaking and budding, seedless fruits, and seed germination. They do the last by breaking the seed’s dormancy and acting as a chemical messenger. Its hormone binds to a receptor, and Ca2+ activates the protein calmodulin, and the complex binds to DNA, producing an enzyme to stimulate growth in the embryo.
A major effect of gibberellins is the degradation of DELLA proteins, the absence of which then allows phytochrome interacting factors to bind to gene promoters and regulate gene expression.[7] Gibberellins are thought to cause DELLAs to become polyubiquitinated and, thus, destroyed by the 26S proteasome pathway.[8]
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