1-Aminocyclopropane-1-carboxylic acid (ACC), a biosynthetic precursor of ethylene, has long been proposed to act as a mobile messenger in higher plants. However, little is known about the transport system of ACC. Recently, our genetic characterization of an ACC-resistant mutant with normal ethylene sensitivity revealed that lysine histidine transporter 1 (LHT1) functions as a transporter of ACC. As amino acid transporters might have broad substrate specificity, we hypothesized that other amino acid transporters including LHT1 paralogs might have the ACC-transporter activity. Here, we took a gain-of-function approach by transgenic complementation of lht1 mutant with a selected set of amino acid transporters. When we introduced transgene into the lht1 mutant, the transgenic expression of LHT2, but not of LHT3 or amino acid permease 5 (AAP5), restored the ACC resistance phenotype of the lht1 mutant. The result provides genetic evidence that some, if not all, amino acid transporters in Arabidopsis can function as ACC transporters. In support, when expressed in Xenopus laevis oocytes, both LHT1 and LHT2 exhibited ACC-transporting activity, inducing inward current upon addition of ACC. Interestingly, the transgenic expression of LHT2, but not of LHT3 or AAP5, could also suppress the early senescence phenotypes of the lht1 mutant. Taking together, we propose that plants have evolved a multitude of ACC transporters based on amino acid transporters, which would contribute to the differential distribution of ACC under various spatiotemporal contexts.

Plants sense and integrate diverse stimuli to determine the timing for germination. A smoke compound, 3,4,5-trimethylfuran-2(5H)-one (trimethylbutenolide, TMB), has been identified to inhibit the seed germination of higher plants. To understand the mode of action, we examined various physiological and molecular aspects of the TMB-dependent inhibition of seed germination in Arabidopsis thaliana. The results indicated that the effect of TMB is due to the enhanced physiological dormancy, which is modulated by other dormancy regulatory cues such as after-ripening, stratification, and ABA/GA signaling. In addition, gene expression profiling showed that TMB caused genome-wide transcriptional changes, altering the expression of a series of dormancy-related genes. Based on the TMB-responsive physiological contexts in Arabidopsis, we performed mutant screening to isolate genetic components that underpin the TMB-induced seed dormancy. As a result, the TMB-RESISTANT1 (TES1) gene in Arabidopsis, encoding a B2 group Raf-like kinase, was identified. Phenotypic analysis of the tes1 mutant implicated that TES1 has a critical role in the TMB-responsive gene expression and the inhibition of seed germination. Taken together, we propose that plants have been equipped with a TMB sensory pathway through which the TMB induces the seed dormancy in a TES1-dependent way.

Light is an important environmental cue, causing a high degree of developmental plasticity in higher plants. The outcome of light-regulated developmental response is determined by not only photosensory systems but also endogenous physiological contexts in plants. functions as a receptor of karrikin and endogenous, as yet to be identified, KAI2 ligand (KL). The loss-offunction of KAI2 caused light-hyposensitive photomorphogenesis, affecting the expression lightresponsive genes under the light conditions. However, it remains still unclear how KAI2-KL signaling interacts with light-signaling. Here, we show that the ply2 mutation, a severe loss-of-function allele of KAI2 affected the expression of a subset of light-responsive genes, irrespectively of light condition. The results implied that the overlapping set of light-and KAI2-responsive genes may serve as an integrating node between light-and KAI2-KL signaling. Further, the results of double mutant analyses between the ply2 mutant and mutants of CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1) or LONG HYPOCOTYL IN FAR-RED (HFR1) implicated that KAI2-KL signaling acts at downstream of COP1, largely independently of HFR1. Together, these results suggest that KAI2-KL signaling intersects with a subset of the lightregulatory network, by which plants adjust their photomorphogenic development. ARTICLE HISTORY