Abstract
The formation of a rosette of leaves is a developmentally fundamental process in rosette plants. The rosette is widely adopted by flowering plants, including a significant proportion of vegetable crops. A key event during the life cycle of rosette plants is the switch from rosette to stem habit in a
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process called bolting. Architecturally, the rosette, where internode elongation is repressed, and the stem, where internode elongation is promoted, are opposites. In rosette crops, such as lettuce, cabbage and beetroot, premature bolting has a negative impact on crop yield, yet molecular regulation of rosette formation and the initiation of bolting are largely unknown. It is known that auxin, gibberellin (GA) and brassinosteroid (BR) phytohormones promote stem elongation, but they do not affect rosette internodes. This suggests that during vegetative growth a regulatory mechanism is in place that prevents internode elongation.
In this thesis we show that the BEL1-LIKE HOMEODOMAIN (BLH) transcription factor ARABIDOPSIS THALIANA HOMEOBOX 1 (ATH1) is a crucial component of such a mechanism in the rosette plant Arabidopsis thaliana. ATH1 is expressed in the shoot apical meristem (SAM) and rib zone (RZ) during vegetative growth, but is downregulated upon bolting. The RZ is inactive during vegetative growth, while bolting requires RZ activity. We show that downregulation of ATH1 is correlated with expansion of the RZ and bolting, while loss of ATH1 during vegetative growth leads to precocious RZ elongation and elongation of rosette internodes (heterochronic bolting). In combination with application of the bolting hormone GA, loss of ATH1 leads to complete loss of rosette habit. Besides GA, heterochronic bolting of ath1 is enhanced by far-red light, high ambient temperature, auxin and BR. Individually, none of these signals affect wild-type rosette internodes. Loss of GA or BR biosynthesis, or the transcription factors WUSCHEL, PHYTOCHROME INTERACTING FACTOR 4 (PIF4), PIF7 or BIG (partially) restores rosette compactness of ath1, signifying a complex interdependency of several signals in regulating internode elongation. During reproductive growth, ectopic expression of ATH1 represses bolting and this phenotype is not restored by GA, auxin or BR application. Together, our findings show that ATH1 instils a robust block on internode elongation that cannot be bypassed until ATH1 is repressed.
In addition, we show that meristem-organ boundary function is important for maintaining rosette habit. Disruption of boundary genes sensitises plants to heterochronic bolting, notably through loss of the ATH1 targets LATERAL ORGAN BOUNDARIES (LOB) or BLADE ON PETIOLE1 (BOP1) and BOP2. ATH1-mediated repression of internode elongation further requires the ATH1-interaction partners KNOTTED-LIKE FROM ARABIDOPSIS THALIANA 2 (KNAT2), KNAT6 and SHOOT MERISTEMLESS (STM), all of which have previously been linked to boundary formation.
Lastly, we show that a related BLH protein, PENNYWISE (PNY), functions partially redundant with ATH1 as a repressor of internode elongation, in contrast with its established role in promoting internode elongation. Together, our findings contribute to the understanding of the molecular control of the rosette habit and bolting and of the identity of the RZ tissue underlying this developmental switch.
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