Antagonistic activities of cotranscriptional regulators within an early developmental window set FLC expression level

Michael Schon,Michael D. Nodine,Congyao Xu,Catherine Baxter,Caroline Dean,Balaji Enugutti

doi:10.1073/pnas.2102753118

Michael Schon, Michael D. Nodine + Show 4 more

Open Access

https://doi.org/10.1073/pnas.2102753118

Copy DOI

Abstract

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, determine 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 cotranscriptional regulators during an early embryonic developmental window thus set FLC expression levels and determine flowering time.

Highlights

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
FLC was the most significantly up-regulated gene in Col FRI embryos, reaching higher transcript abundance at the early heart stage than any timepoint measured during Col-0 embryo development (Fig. 1 D and E and Dataset S2) [11]
We find that FCA promotes proximal polyadenylation of the sense nascent FLC transcript in

Summary

Introduction

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. We show that antagonistic functions of the FLC activator FRIGIDA (FRI) and the repressor FCA, at a specific stage of embryo development, determine FLC expression and flowering. FRI antagonizes an FCA-induced proximal polyadenylation to increase FLC expression and delay flowering. Opposing functions of cotranscriptional regulators during an early embryonic developmental window set FLC expression levels and determine flowering time. We show that they antagonistically regulate polyadenylation site usage of the FLC nascent transcript within an early developmental window during embryo development. This establishes an expression state that is maintained by a Polycomb mechanism during the rest of development

Methods

Results

Conclusion