High impact information on TFL1

• FT acts in part downstream of CO and mediates signals for flowering in an antagonistic manner with its homologous gene, TERMINAL FLOWER1 (TFL1) [1].
• FT, and likely also TFL1, is recruited to the promoters of floral genes through interaction with FD, a bZIP transcription factor [2].
• We show here that this negative regulation can be mutual because TFL1 expression is downregulated in plants constitutively expressing AP1 [3].
• Shoot meristems maintain an identity distinct from that of flower meristems, in part through the action of genes such as TERMINAL FLOWER1 (TFL1), which bars AP1 and LFY expression from the influorescence shoot meristem [3].
• We suggest that the wild-type pattern of TERMINAL FLOWER 1 and floral meristem identity gene expression depends on the relative timing of their upregulation [4].

Biological context of TFL1

• These lines implicate divergence of LcrLFY cis-regulation as the primary cause of both novel transgenic phenotypes but implicate divergence of LcrLFY protein function as the primary cause of elevated TFL1 levels [5].
• Taken together these results show that LcrLFY has diverged from A. thaliana in both the cis-regulatory and protein-coding regions and imply that molecular coevolution of LcrLFY and the L. crassa TFL1 ortholog, LcrTFL1, contributed to the evolution of rosette flowering [5].
• In our tfl1 mutant, no nucleotide substitution was found in the transcribed region of the gene, and the T-DNA-insertion site was located at 458 bp downstream of the putative polyadenylation signal, suggesting that an element important for expression of the TFL1 gene exists in this area [6].
• Nucleotide sequences of the region homologous to this putative TFL1 gene were compared between five chemically induced tfl1 mutants and their parental wild-type ecotypes [6].
• The deduced amino acid sequence of CsTFL was 65% identical to the Arabidopsis TFL1 protein [7].

Other interactions of TFL1

• In combination, these results identify a molecular surface likely to be recognized by FT- and/or TFL1-specific interactors [2].
• The enhanced phenotype of the double mutant suggests that TFL2 acts in a developmental pathway distinct from TFL1 [8].
• In contrast, the coding regions of TFL1 and LFY display a significant reduction in nucleotide variation, suggesting that these sequences have been subjected to a recent adaptive sweep [9].
• Constitutive overexpression of RCN1 or RCN2 in Arabidopsis caused a late-flowering and highly branching phenotype, indicating that they possess conserved biochemical functions as TFL1 [10].
• However, in contrast to TFL1, the expression of ATC was only detected in the hypocotyl of young plants, and not in the IM [11].

References