Flowering time of plants must be tightly regulated to maximize reproductive success. Plants have evolved sophisticated signaling network to coordinate the timing of flowering in response to their ever-changing environmental conditions. Besides being a key immune signal, the lipid-derived plant hormone jasmonate (JA) also regulates a wide range of developmental processes including flowering time. Here, we report that the CORONATINE INSENSITIVE1 (COI1)-dependent signaling pathway delays the flowering time of Arabidopsis thaliana by inhibiting the expression of the florigen gene FLOWERING LOCUS T (FT). We provide genetic and biochemical evidence that the APETALA2 transcription factors (TFs) TARGET OF EAT1 (TOE1) and TOE2 interact with a subset of JAZ (jasmonate-ZIM domain) proteins and repress the transcription of FT. Our results support a scenario that, when plants encounter stress conditions, bioactive JA promotes COI1-dependent degradation of JAZs. Degradation of the JAZ repressors liberates the transcriptional function of the TOEs to repress the expression of FT and thereby triggers the signaling cascades to delay flowering. Our study identified interacting pairs of TF and JAZ transcriptional regulators that underlie JA-mediated regulation of flowering, suggesting that JA signals are converted into specific context-dependent responses by matching pairs of TF and JAZ proteins.

BackgroundFruit maturation and ripening are genetically regulated processes that involve a complex interplay of plant hormones, growth regulators and multiple biological and environmental factors. Tomato (Solanum lycopersicum) has been used as a model of biological and genetic studies on the regulation of specific ripening pathways, including ethylene, carotenoid and cell wall metabolism. This model has also been used to investigate the functions of upstream signalling and transcriptional regulators. Thus far, many ripening-associated transcription factors that influence fruit development and ripening have been reported. NAC transcription factors are plant specific and play important roles in many stages of plant growth and development, such as lateral root formation, secondary cell wall synthesis, and embryo, floral organ, vegetative organ and fruit development.ResultsTissue-specific analysis by quantitative real-time PCR showed that SlNAC1 was highly accumulated in immature green fruits; the expression of SlNAC1 increased with fruit ripening till to the highest level at 7 d after the breaker stage. The overexpression of SlNAC1 resulted in reduced carotenoids by altering carotenoid pathway flux and decreasing ethylene synthesis mediated mainly by the reduced expression of ethylene biosynthetic genes of system-2, thus led to yellow or orange mature fruits. The results of yeast one-hybrid experiment demonstrated that SlNAC1 can interact with the regulatory regions of genes related lycopene and ethylene synthesis. These results also indicated that SlNAC1 inhibited fruit ripening by affecting ethylene synthesis and carotenoid accumulation in SlNAC1 overexpression lines. In addition, the overexpression of SlNAC1 reduced the firmness of the fruits and the thickness of the pericarp and produced more abscisic acid, resulting in the early softening of fruits. Hence, in SlNAC1 overexpression lines, both ethylene-dependent and abscisic acid-dependent pathways are regulated by SlNAC1 in fruit ripening regulatory network.ConclusionsSlNAC1 had a broad influence on tomato fruit ripening and regulated SlNAC1 overexpression tomato fruit ripening through both ethylene-dependent and abscisic acid-dependent pathways. Thus, this study provided new insights into the current model of tomato fruit ripening regulatory network.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-014-0351-y) contains supplementary material, which is available to authorized users.

No abstract

No abstract

No abstract