GIBBERELLINS REGULATE CELL DIVISION AND PARTHENOCARPIC FRUIT SET IN CITRUS

Fruit set and growth is regulated by hormones interaction, gibberellins (GA) being a main part of the process in Citrus. Actually, it is well known the time-course of GA content in the citrus ovary during flowering and its correlation with fruit set in both seeded and seedless species. However, GA endogenous role is uncertain. Is GA in the ovary a direct regulator or an indirect part of the hormonal stimuli that reactivates and maintains cell division triggering fruit set? While in seeded varieties GA synthesis that occurs in fertilized ovules is the primary stimulus controlling early ovary development, is there any specific tissue-dependent regulation of parthenocarpy? While initiation of GA synthesis is thought to be autonomous in the sterile parthenocarpic species, it is unclear whether it is autonomous or stimulated in the fertile self-incompatible species, which present a wide variation in their parthenocarpic ability. Attending to the aforementioned, in this PhD Thesis, the following hypothesis was tested: The autonomous synthesis of GA in the pericarp directly activates and maintains cell division in the ovary, promoting the flower to fruit transition in parthenocarpic Citrus. The main findings are: 1. In the parthenocarpic cultivars, GA biosynthesis is first located in the whole pericarp and the ovules during the flower to fruit transition; later, during the fruit cell division developmental stage, GA biosynthesis is located in the endocarp and growing juice sacs. 2. The autonomous activation of GA biosynthesis directly stimulates CYCA1,1 gene expression and cell division in the ovary walls (exocarp and mainly mesocarp) and in the endocarp (growing juice sacs), increasing ovary growth rates and leading to higher parthenocarpic fruit set. 3. Fertile self-incompatible cultivars (i.e. Clementine mandarins) present pollination-independent facultative parthenocarpy, rather than stimulative parthenocarpy, with its ability to set being dependent on endogenous GA1 levels in the ovary at anthesis, which is triggered autonomously depending on the genotype.