Introduction

Many theories to explain the generation of floret pattern in capitula of Compositae have been developed (Schwabe, 1984; Hernández, 1988; Green, 1991; Hernández and Green, 1993; Jean, 1994). Nevertheless the processes involved in the differentiation and pattern generation of floret primordia are not yet well understood.
This paper reports the changes produced in the floret pattern in the capitulum of sunflower using the morphactin Chlorflurenol (CF1: 2-Chloro-9-Hydroxy-fluorene-9-Carboxylic acid) which main action, produced by the inhibition of IAA transport (Noodén and Noodén, 1985), is the reduction of meristematic growth (Schneider, 1970).

Materials and Methods

Sunflower plants (Helianthus annuus L.) cv. Sunfola 68-2 were grown under controlled environmental conditions (18 h long-day photoperiod, 500 mmol s^-1 m^-2 PPFD at the canopy level, 28 °C day-night temperature) in 2 L plastic pots containing garden soil. Plants were periodically watered and fertilized to ensure optimal level of nutrients. Startinf at Floral Stage (FS) 4 (Marc and Palmer, 1981), three applications of CFI were made at daily intervals, spraying the plants with an aq. solution of 50 mg L^-1 of CFI in ethanol 20% (v/v), providing a dose of 250 mg of CFL per plant.day^-1. Control plants were similarly sprayed with a 20% (v/v) ethanol solution.
Capitula were dissected at daily intervals, fixed and processed for SEM [critical point dried, mounted on metal stubs and sputter coated with gold, examined in a Cambridge S4-10 SEM at 20 kV and photographed] or light microscopy [embedded in LR White acrylic resin, sectioned at 1-2 mm using glass knives, the sections stained with Fluorescent Brightener 28 (Hernández and Palmer, 1988) and observed with UV light].

Results and Conclusion

The action of CFL was reflected in a complete inhibition of floret development resulting in a barren area at the receptacle center (Fig. 1A-B). The morphology of developing florets was modified and the floret corolla reduced to a "cup shaped" structure (Fig. 1B). The orderly initiation of floret primordia was also disrupted (Fig. 1B).
The capitula did not lose its capacity to expand (Fig 1A-B) and compared with the controls, the receptacle sizes were only reduced at 12-15 %. This suggests that CF1 does not arrest anticlinal cell divisions in the tunica layer (Hernández, 1988). Moreover, some periclinal divisions were also observed in the tunica layer (Fig. 1C) resulting in the development of hairs in the central area of some capitula (Fig. 1D). Plants allowed to grow for a further 5-10 days, did not show any symptoms of recovery from the CF1 -treatment and the production of floret primordia remained suspended. Control plants (not presented in this paper) showed normal development of floret primordia at the time of sampling.
CF1 curtailed the mitotic activity of the corpus so altering the sub surface activity (Fig. 1C) that accompanies the formation of primordia. Then, if applied in the transitional phase of flowering (i.e. EF4), CFL causes inhibition of floret production and differentiation by arresting periclinal cell divisions at the receptacle sub-surface level. Changes observed in the floret primordia pattern can be used to further study the way in which this pattern is naturally generated in a normal capitulum.

References

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