TERMINAL FLOWER 1-FD complex target genes and competition with FLOWERING LOCUS T

Yang Zhu,Koji Goto,Doris Wagner,Cheol Woong Jeong,Run Jin,Samantha Klasfeld,Nobutoshi Yamaguchi

doi:10.1038/s41467-020-18782-1

Abstract

Plants monitor seasonal cues to optimize reproductive success by tuning onset of reproduction and inflorescence architecture. TERMINAL FLOWER 1 (TFL1) and FLOWERING LOCUS T (FT) and their orthologs antagonistically regulate these life history traits, yet their mechanism of action, antagonism and targets remain poorly understood. Here, we show that TFL1 is recruited to thousands of loci by the bZIP transcription factor FD. We identify the master regulator of floral fate, LEAFY (LFY) as a target under dual opposite regulation by TFL1 and FT and uncover a pivotal role of FT in promoting flower fate via LFY upregulation. We provide evidence that the antagonism between FT and TFL1 relies on competition for chromatin-bound FD at shared target loci. Direct TFL1-FD regulated target genes identify this complex as a hub for repressing both master regulators of reproductive development and endogenous signalling pathways. Our data provide mechanistic insight into how TFL1-FD sculpt inflorescence architecture, a trait important for reproductive success, plant architecture and yield.

Highlights

Plants monitor seasonal cues to optimize reproductive success by tuning onset of reproduction and inflorescence architecture
Biochemical and genetic studies showed that FLOWERING LOCUS T (FT) physically interacts with the bZIP transcription factor FD via 14-3-3 proteins and similar interactions have recently been described for TFL119–22
A key unanswered question is how the florigens modulate plant form—what are the downstream processes they set in motion and what is molecular basis for their antagonism? Here we show that TERMINAL FLOWER 1 (TFL1) is recruited to target loci by the bZIP transcription factor FD

Summary

Result

TFL1 is recruited to thousands of loci by the bZIP transcription factor FD. Mechanistic insight into TFL1 activity has been hampered by low protein abundance. The bZIP-binding site mutations in the second exon of LFY in addition strongly reduced reporter expression in incipient and young flower primordia Genes encoding promoters of floral fate[32] (LFY, AP1, FUL and LMI2) clustered together (cluster III in Fig. 5c) and displayed stronger upregulation in tfl[1] mutants than in the wild type This pattern of de-repression was confirmed for all four loci using independent biological samples and qRT-PCR (Supplementary Fig. 12a). The identified indirect targets provide a ‘molecular phenotype’ that is consistent with de-repression of the auxin, brassinosteroid and cytokinin hormone pathways upon FRP treatment in the wild-type and in tfl[1] mutants (Fig. 5c). Regulators and chromatin regulators among the direct TFL1–FD repressed targets (Supplementary Fig. 14a, b)

Discussion

Methods

Findings

Code availability