A series of activities antagonistically regulate FLC expression levels in ambient temperatures.
FRIGIDA (FRI) activates FLC whereas the autonomous promotion pathway components repress FLC expression.
FRI molecular function is still unclear but it involves interaction with the cap-binding complex and increases H3K4me3 and H3 acetylation at FLC. Independent loss of function of FRI has led to the recurrent evolution of a rapid-cycling habit Arabidopsis accessions.
The genetically defined autonomous pathway identifies a series of interconnecting functions that repress FLC expression.
Activities of proteins such as FCA, FY, FPA influence co-transcriptional processing of FLC antisense transcripts. This reduces transcription of the sense strand in a mechanism requiring FLD, a histone K4 me2 demethylase. Computational modelling has helped reveal this pathway co-ordinately affects transcription initiation and elongation rate.
FRIGIDA and the autonomous pathway have genome-wide functions in Arabidopsis. FCA and FPA function in promoting proximal polyadenylation of many transcripts, limiting intergenic transcription.
The Dean lab are investigating these co-transcriptional functions, how they interact with RNA silencing pathways and their involvement with stabilisation and removal of RNA:DNA hybrids (R-loops) in the genome.