Genetic interactions reveal the antagonistic roles of FT/TSF and TFL1 in the determination of inflorescence meristem identity in Arabidopsis

Abstract

Summary During the transition to the reproductive phase, the shoot apical meristem switches from the developmental program that generates vegetative organs to instead produce flowers. In this study, we examined the genetic interactions of FLOWERING LOCUS T (FT)/TWIN SISTER OF FT (TSF) and TERMINAL FLOWER 1 (TFL1) in the determination of inflorescence meristem identity in Arabidopsis thaliana. The ft‐10 tsf‐1 mutants produced a compact inflorescence surrounded by serrated leaves (hyper‐vegetative shoot) at the early bolting stage, as did plants overexpressing TFL1. Plants overexpressing FT or TSF (or both FT and TFL1) generated a terminal flower, as did tfl1‐20 mutants. The terminal flower formed in tfl1‐20 mutants converted to a hyper‐vegetative shoot in ft‐10 tsf‐1 mutants. Grafting ft‐10 tsf‐1 or ft‐10 tsf‐1 tfl1‐20 mutant scions to 35S::FT rootstock plants produced a normal inflorescence and a terminal flower in the scion plants, respectively, although both scions showed similar early flowering. Misexpression of FT in the vasculature and in the shoot apex in wild‐type plants generated a normal inflorescence and a terminal flower, respectively. By contrast, in ft‐10 tsf‐1 mutants the vasculature‐specific misexpression of FT converted the hyper‐vegetative shoot to a normal inflorescence, and in the ft‐10 tsf‐1 tfl1‐20 mutants converted the shoot to a terminal flower. TFL1 levels did not affect the inflorescence morphology caused by FT/TSF overexpression at the early bolting stage. Taking these results together, we proposed that FT/TSF and TFL1 play antagonistic roles in the determination of inflorescence meristem identity, and that FT/TSF are more important than TFL1 in this process.

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

“…This is expected since the bZIP mutations at the LFY locus prevent access of both TFL1 and of activating PEBP family members FT and the closely related TWIN SISTER OF FT (TSF). Indeed, it has been shown that the terminal flower phenotype of tfl1 is suppressed in tfl1 ft tsf triple mutants 49 .…”

Prospects for the accelerated improvement of the resilient crop quinoa

“…The role of FT in flowering is mainly counteracted by the action of TERMINAL FLOWER 1 ( TFL1 ), a close homologue belonging to the CENTRORADIALIS (CEN)-like subfamily of proteins. Indeed, FT and TFL1 have antagonistic roles in the regulation of flowering across different plant species ( Seo et al , 2009 ; Pin et al , 2010 ; Wickland and Hanzawa, 2015 ; Wang et al , 2017 ; Kaneko-Suzuki et al , 2018 ; Lee et al , 2019 ; Wu et al , 2019 ). In Arabidopsis, rice, and soybean ( Glycine max ), TFL1 loss-of-function mutations cause early flowering and the generation of a terminal inflorescence ( Shannon and Meeks-Wagner, 1991 ; Liu et al , 2010 ; Repinski et al , 2012 ; Kaneko-Suzuki et al , 2018 ).…”

“…In Arabidopsis, rice, and soybean ( Glycine max ), TFL1 loss-of-function mutations cause early flowering and the generation of a terminal inflorescence ( Shannon and Meeks-Wagner, 1991 ; Liu et al , 2010 ; Repinski et al , 2012 ; Kaneko-Suzuki et al , 2018 ). At least in Arabidopsis and rice, FT proteins activate the expression of flowering genes, while members of the TFL1 protein family are involved in the transcriptional repression of genes activated by FT ( Kaneko-Suzuki et al , 2018 ; Lee et al , 2019 ). If a similar mechanism operates in quinoa, generating TFL1 loss-of-function mutations might be a simple alternative to FT mutagenesis to achieve early flowering phenotypes.…”

Functional characterization of mungbean CONSTANS-LIKE genes reveals a key role for CONSTANS-LIKE 2 in the control of flowering time in A. thaliana under short-day conditions

“…These include the photoperiodic, vernalization, ambient temperature, plant hormone, and autonomous owering pathways [1,[4][5][6][7][8][9][10]. Within these pathways, a number of genes have been identi ed as involved in owering time regulation, including CONSTANS-LIKE (COL) genes, phosphatidyl ethanolamine-binding protein (PEBP) genes and several members of MADS-Box gene family [1][2][11][12][13][14][15][16][17][18][19].…”