Antagonistic activities of cotranscriptional regulators within an early developmental window set <i>FLC</i> expression level.

Abstract

Quantitative variation in expression of the <i>Arabidopsis</i> floral repressor <i>FLC</i> influences whether plants overwinter before flowering, or have a rapid cycling habit enabling multiple generations a year. Genetic analysis has identified activators and repressors of <i>FLC</i> expression but how they interact to set expression level is poorly understood. Here, we show that antagonistic functions of the <i>FLC</i> activator FRIGIDA (FRI) and the repressor FCA, at a specific stage of embryo development, determine <i>FLC</i> expression and flowering. FRI antagonizes an FCA-induced proximal polyadenylation to increase <i>FLC</i> expression and delay flowering. Sector analysis shows that FRI activity during the early heart stage of embryo development maximally delays flowering. Opposing functions of cotranscriptional regulators during an early embryonic developmental window thus set <i>FLC</i> expression levels and determine flowering time.