The transition from vegetative development to flowering is a major event in the life cycle of plants. Stem cells in the shoot apical meristem switch from producing primordia that will give rise to the vegetative parts of the plant (e.g. leaves) to produce the reproductive structures (flowers). Because proper timing of this transition is critical to reproductive success, it is highly regulated by both environmental and endogenous factors. One major pathway that regulates flowering time is the autonomous floral-promotion pathway (AP). This pathway promotes flowering by repressing expression of FLOWERING LOCUS C (FLC), a MADS-domain-containing transcription factor that acts to delay flowering. The AP is comprised of seven genes that are predicted to encode three RNA-binding proteins (FCA, FPA, and FLK), a polyadenylation factor (FY), two components of the histone deacetylase complex (FLD and FVE), and a homeodomain-containing transcription factor (LD). Null mutations in any one of the AP genes results in increased FLC expression and delayed flowering, thus the activity of all seven genes is required for FLC repression. Currently little is known about how this interesting group of genes acts at a molecular level, although the putative functions of the AP proteins suggests a possible link between RNA processing and chromatin structure;this is an exciting possibility given that other pathways are known to epigenetically regulate FLC through histone modifications.
Our specific aims, therefore, are designed to gain4nsight in to the moteeulaf mechanism ofttieAP;The knowledge gained in these studies is likely to have impacts both in and outside of plant research. Examples of RNA molecules playing key roles in regulating chromatin structure are found from yeast to humans, yet the molecular mechanisms of these phenomenons are not well understood. Thus the insights gained in this work could have impacts across the eukaryotic kingdom.
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