TERMINAL FLOWER1 Acts in Transcriptional Repression

In the study of flowering, much attention focuses on FLOWERING LOCUS T (FT), the mobile protein produced in leaves and transported to the shoot apical meristem to activate flowering. However, an equally important focus is the checks that prevent premature initiation of flowering. Some repressors of flowering, such as the MADS domain transcription factor FLOWERING LOCUS C, act on FT to prevent its expression (reviewed in Yant et al., 2009). One intriguing repressor, TERMINAL FLOWER1 (TFL1), shows very high amino acid sequence similarity to FT but acts opposite to FT. For example, plants overexpressing FT show a similar phenotype to tfl1 mutant plants; both have terminal flowers in their inflorescences, in contrast with wild-type Arabidopsis, which maintains an indeterminate inflorescence meristem that continues to produce new flowers. Neither FT nor TFL1 has discernable transcription factor domains. FT promotes flowering by interacting with the bZIP transcription factor FD to activate transcription of key flowering genes such as APETALA1 and LEAFY.

To address the question of whether TFL1 also acts in transcriptional regulation, Hanano and Goto (pages 3172–3184) made two protein fusions, fusing TFL1 with the transcriptional activation domain VP16 and the transcriptional repression domain SRDX. The authors predicted that if TFL1 acts in transcription, these domains will affect its function. Indeed, the TFL1-SRDX fusion acted in the same mode as the native TFL1, complementing the terminal flower phenotype of tfl1 mutants. By contrast, TFL1-VP16 produced a dominant-negative terminal flower phenotype similar to tfl1 mutants (see figure). These results indicated that TFL1 acts in transcriptional repression, as its fusion to the repressor domain SRDX recapitulated native TFL1 function. To address the next question, whether it acts on the same targets as FT, or on a parallel pathway, to suppress flowering, the authors next examined the mRNA levels of a set of target genes regulated by FT. They found that a set of five FT targets all showed lower levels in the TFL1-SRDX plants, indicating that TFL1 acts opposite to FT by acting on the same targets, rather than on a separate set of targets. Moreover, they found that TFL1 also acts through FD, as fd mutants partially or completely suppressed both tfl1 mutants and the dominant-negative effect of TFL1-VP16. Indeed, the authors also showed by bimolecular fluorescence complementation that TFL1 and FD interact in the nucleus. Thus, TFL1 acts with FD to repress floral identity genes that are also FT targets. The exact mechanism of this action remains an interesting topic for future study.

TFL1 regulates flowering via transcriptional repression. Left to right: Col, tfl1-17, 35S:TFL1-VP16/Col, and 35S:TFL1-VP16/tfl1-17 plants at 6 weeks. Inset: 35S:TFL1-VP16/Col inflorescence, with terminal flower (TF). Bar =1 cm and 1 mm in the inset. (Reprinted from Figure 2 of Hanano and Goto [2011].)