Background: Flowering is a key process in the life cycle of plants. The transition from vegetative to reproductive growth is thus under sophisticated regulation by endogenous and environmental signals. The plant-specific Teosinte Branched 1/Cycloidea/Proliferating Cell Factors (TCP) family transcription factors are involved in many biological processes, but their roles in regulating flowering have not been totally elucidated. Results: We explored the role of Arabidopsis TCP8 in plant development and, especially, in flowering control. Overexpression of TCP8 significantly delayed flowering under both long-day and short-day conditions and dominant repression by TCP8 led to various growth defects. The upregulation of TCP8 led to more accumulated mRNA level of FLOWERING LOCUS C (FLC), a central floral repressor of Arabidopsis. TCP8 functions in an FLCdependent manner, as TCP8 overexpression in the flc-6 loss-of-function mutant failed to delay flowering. The vernalization treatment could reverse the late flowering phenotype caused by TCP8 overexpression. Conclusions: Our results provide evidence for a role of TCP8 in flowering control and add to our knowledge of the molecular basis of TCP8 function.

RNA uridylation, catalyzed by terminal uridylyl transferases (TUTases), represents a conserved and widespread posttranscriptional RNA modification in eukaryotes that affects RNA metabolism. In plants, several TUTases, including HEN1 SUPPRESSOR 1 (HESO1) and UTP: RNA URIDYLYLTRANSFERASE (URT1), have been characterized through genetic and biochemical approaches. However, little is known about their physiological significance during plant development. Here, we show that HESO1 and URT1 act cooperatively with the cytoplasmic 3′–5′ exoribonucleolytic machinery component SUPERKILLER 2 (SKI2) to regulate photosynthesis through RNA surveillance of the Calvin cycle gene TRANSKETOLASE 1 ( TKL1 ) in Arabidopsis . Simultaneous dysfunction of HESO1 , URT1 , and SKI2 resulted in leaf etiolation and reduced photosynthetic efficiency. In addition, we detected massive illegitimate short interfering RNAs (siRNAs) from the TKL1 locus in heso1 urt1 ski2 , accompanied by reduced TKL1/2 expression and attenuated TKL activities. Consequently, the metabolic analysis revealed that the abundance of many Calvin cycle intermediates is dramatically disturbed in heso1 urt1 ski2 . Importantly, all these molecular and physiological defects were largely rescued by the loss-of-function mutation in RNA-DEPENDENT RNA POLYMERASE 6 ( RDR6 ), demonstrating illegitimate siRNA-mediated TKL silencing. Taken together, our results suggest that HESO1- and URT1-mediated RNA uridylation connects to the cytoplasmic RNA degradation pathway for RNA surveillance, which is crucial for TKL expression and photosynthesis in Arabidopsis .

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