A longstanding question in plant biology is how plants "decide" when to flower. Plants go through successive phases in their lifecycle. During vegetative development plants convert the energy from sunlight into resources. When plants switch to flowering, the accumulated resources are incorporated into the seeds. As a consequence, the timing of flowering impacts both plant biomass production (biofuel production) and the number of fruits and seeds produced (yield). Plants adjust the time to flower formation based on environmental cues, most importantly the season of the year and the temperature. When seasonal cues are optimal for flowering, plants produce a substance called "florigen". Florigen moves throughout the plant and triggers production of flowers. A closely related substance named "antiflorigen" prevents flower formation in the absence of the seasonal cue. Despite its important function, it is not understood how antiflorigen prevents flowering, nor how antiflorigen activity is overcome to allow flower formation. The proposed activities will address these deficiencies. Insight gained can be used to enhance desirable traits in crop species. The research will be discussed with the general public in conjunction the national citizen science "Project Bud Burst" at the Morris Arboretum. Contributions to enhancing high school education will be made through lectures and workshops during the yearly high school summer research academy and hands on teacher professional development. Finally, undergraduates will be engaged in research related to the role and regulation of antiflorigen in laboratory classes and in the research lab.
This proposal will address two general questions. The first is how TFL1 represses onset of flower formation. Using chromatin immunoprecipitation (ChIP) and analysis of gene expression, the proposal will identify the genes directly repressed by the antiflorigen TFL1 prior to the onset of flower formation. Both candidate gene and unbiased genomic approaches will be employed. Follow-up molecular and genetic studies will assess the biological contribution of the TFL1 target genes to TFL1 function. Finally, the proposed activities will elucidate how TFL1 is recruited to its target loci. The second question to be addressed is how TFL1-mediated repression is overcome to allow formation of the first flower upon perception of inductive cues. Using biochemical, genetic and genomic approaches, the proposed activities will test the hypothesis that competition by the FT florigen for access to shared target loci and subsequent negative feedback by LFY and AP1 on TFL1 expression play critical roles in this process. Mathematical modeling will be used to determine whether the uncovered interactions explain the behavior of the system.
