Date of Award

Summer 2011

Degree Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Graduate Group

Biology

First Advisor

Doris Wagner

Abstract

The switch from producing vegetative structures--branches and leaves--to producing reproductive structures--flowers--is a crucial developmental transition that significantly affects the reproductive success of flowering plants. In Arabidopsis thaliana , this transition is in large part controlled by the meristem identity regulator LEAFY (LFY) and the LFY direct target APETALA1 (AP1 ). The molecular mechanisms by which LFY orchestrates a precise and robust switch to flower formation is not well understood. Here we show that the R2R3 MYB transcription factor and direct LFY target LATE MERISTEM IDENTITY2 ( LMI2 ) plays a role in the meristem identity transition. Like LFY, LMI2 directly activates AP1 ; moreover LMI2 and LFY physically interact. LFY, LMI2 and AP1 are connected in a feed-forward and positive feedback loop network. We propose that these intricate regulatory interactions direct not only the precision of this critical developmental transition, but also contribute to its robustness and irreversibility.

Subsequent to the meristem identity transition floral primordia undergo a growth period prior to floral organogenesis. This growth phase is maintained in part by the flowering-time genes SHORT VEGETATIVE PHASE (SVP), AGAMOUS-LIKE24 (AGL24) and SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1). Eventually, these flowering-time genes are downregulated by AP1. This downregulation results in the termination of meristematic activity and the onset of floral differentiation. In the absence of AP1, ectopic expression of SVP, AGL24 and SOC1 prevents differentiation and leads to the development of floral meristems in the axils of the first whorl organs. These floral meristems give rise to "branched" flowers. Here we present a possible role for LMI2 during floral primordia growth. Similar to SVP, AGL24 and SOC1, AP1 downregulates LMI2 in young flower primordia thus preventing the development of branched flowers. LMI2 acts in the same pathway as SVP, AGL24 and SOC1 and the similar expression patterns of LMI2 and SVP as well as the direct binding of LMI2 to SVP suggests a link between LMI2 and the pathways that maintain primordia growth during early flower development.

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