Leaves start to develop at the peripheral zone of the shoot apical meristem. Thereafter, symmetric and flattened leaf laminae are formed. These events are simultaneously regulated by auxin, transcription factors, and epigenetic regulatory factors. However, the relationships among these factors are not well known. In this study, we conducted protein-protein interaction assays to show that our previously reported Leaf and Flower Related (LFR) physically interacted with SWI3B, a component of the ATP-dependent chromatin remodeling SWI/SNF complex in Arabidopsis. The results of truncated analysis and transgenic complementation showed that the N-terminal domain (25–60 amino acids) of LFR was necessary for its interaction with SWI3B and was crucial for LFR functions in Arabidopsis leaf development. Genetic results showed that the artificial microRNA knockdown lines of SWI3B (SWI3B-amic) had a similar upward-curling leaf phenotype with that of LFR loss-of-function mutants. ChIP-qPCR assay was conducted to show that LFR and SWI3B co-targeted the promoters of YABBY1/FILAMENTOUS FLOWER (YAB1/FIL) and IAA carboxyl methyltransferase 1 (IAMT1), which were misexpressed in lfr and SWI3B-amic mutants. In addition, the association between LFR and the FIL and IAMT1 loci was partly hampered by the knockdown of SWI3B. These data suggest that LFR interacts with the chromatin-remodeling complex component, SWI3B, and influences the transcriptional expression of the important transcription factor, FIL, and the auxin metabolism enzyme, IAMT1, in flattened leaf lamina development.

The success of plant reproduction depends on the timely transition from the vegetative phase to reproductive growth, a process often referred to as flowering. Although several plant-specific transcription factors belonging to the Teosinte Branched 1/Cycloidea/Proliferating Cell Factor (TCP) family are reportedly involved in the regulation of flowering in Arabidopsis, the molecular mechanisms, especially for Class I TCP members, are poorly understood. Here, we genetically identified Class I TCP7 as a positive regulator of flowering time. Protein interaction analysis indicated that TCP7 interacted with several Nuclear Factor-Ys (NF-Ys), known as the 'pioneer' transcription factors; CONSTANS (CO), a main photoperiod regulator of flowering. SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1) was differentially expressed in the dominant-negative mutant of TCP7 (lcu) and the loss-of-function mutant of Class I TCP members (septuple). Additionally, we obtained genetic and molecular evidence showing that TCP7 directly activates the flowering integrator gene, SOC1. Moreover, TCP7 synergistically activated SOC1 expression upon interacting with CO and NF-Ys in vivo. Collectively, our results provide compelling evidence that TCP7 synergistically interacts with NF-Ys to activate the transcriptional expression of the flowering integrator gene SOC1.