Antagonistic activities of co-transcriptional regulators within an early developmental window sets quantitative FLC expression. Antagonistic activities of co-transcriptional regulators within an early developmental window sets quantitative FLC expression

Quantitative variation in expression of the Arabidopsis floral repressor FLC 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 FLC expression, but how they interact to set expression level is poorly understood. Here, we show that antagonistic functions of the FLC activator FRIGIDA (FRI), and the repressor FCA, at a specific stage of embryo development, determines FLC expression and flowering. FRI antagonizes an FCA-induced proximal polyadenylation to increase FLC expression and delay flowering. Sector analysis shows that FRI activity during the early heart stage of embryo development maximally delays flowering. Opposing functions of co-transcriptional regulators during an early embryonic developmental window thus set FLC expression levels and determine flowering time. Overall design: mRNA-seq libraries were constructed for three biological replicates of early heart stage embryos from three genotypes

拟南芥开花抑制因子FLC（Flowering Locus C）的表达量量化差异，会影响植物是否需经过越冬后再开花，或是呈现快速循环的生长习性，从而实现一年多代繁殖。
遗传学分析已鉴定出FLC表达的激活因子与抑制因子，但对于这些因子如何协同调控以确定FLC的表达水平，目前仍知之甚少。
本研究发现，在胚胎发育的特定阶段，FLC的激活因子FRIGIDA（FRI）与抑制因子FCA之间的拮抗作用，决定了FLC的表达水平与开花进程。
FRI通过拮抗FCA诱导的近端多聚腺苷酸化过程，提升FLC的表达量并延迟开花。
嵌合分析显示，在胚胎发育早期心形胚阶段发挥FRI活性，可最大程度地延迟开花。
因此，共转录调控因子在早期胚胎发育窗口期的拮抗作用，共同确定了FLC的表达水平，并最终决定了植物的开花时间。
实验设计概要：针对3种基因型的早期心形胚阶段胚胎，构建了3个生物学重复的mRNA测序文库。