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Background: Riboflavin is the precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), essential cofactors for many metabolic enzymes that catalyze a variety of biochemical reactions. Previously we showed that free flavin (riboflavin, FMN, and FAD) concentrations were decreased in leaves of transgenic Arabidopsis plants expressing a turtle riboflavin-binding protein (RfBP). Here, we report that flavin downregulation by RfBP induces the early flowering phenotype and enhances expression of floral promoting photoperiod genes., Results: Early flowering was a serendipitous phenomenon and was prudently characterized as a constant phenotype of RfBP-expressing transgenic Arabidopsis plants in both long days and short days. The phenotype was eliminated when leaf free flavins were brought back to the steady-state levels either by the RfBP gene silencing and consequently nullified production of the RfBP protein, or by external riboflavin feeding treatment. RfBP-induced early flowering was correlated with enhanced expression of floral promoting photoperiod genes and the florigen gene FT in leaves but not related to genes assigned to vernalization, autonomous, and gibberellin pathways, which provide flowering regulation mechanisms alternative to the photoperiod. RfBP-induced early flowering was further correlated with increased expression of the FD gene encoding bZIP transcription factor FD essential for flowering time control and the floral meristem identity gene AP1 in the shoot apex. By contrast, the expression of FT and photoperiod genes in leaves and the expression of FD and AP1 in the shoot apex were no longer enhanced when the RfBP gene was silenced, RfBP protein production canceled, and flavin concentrations were elevated to the steady-state levels inside plant leaves., Conclusions: Token together, our results provide circumstantial evidence that downregulation of leaf flavin content by RfBP induces early flowering and coincident enhancements of genes that promote flowering through the photoperiod pathway.

Background: It is well known that salt stress has different effects on old and young tissues. However, it remains largely unexplored whether old and young tissues have different regulatory mechanism during adaptation of plants to salt stress. The aim of this study was to investigate whether salt stress has different effects on the ion balance and nitrogen metabolism in the old and young leaves of rice, and to compare functions of both organs in rice salt tolerance., Results: Rice protected young leaves from ion harm via the large accumulation of Na+ and Cl- in old leaves. The up-regulation of OsHKT1;1, OsHAK10 and OsHAK16 might contribute to accumulation of Na+ in old leaves under salt stress. In addition, lower expression of OsHKT1;5 and OsSOS1 in old leaves may decrease frequency of retrieving Na+ from old leaf cells. Under salt stress, old leaves showed higher concentration of NO3- content than young leaves. Up-regulation of OsNRT1;2, a gene coding nitrate transporter, might contribute to the accumulation of NO3- in the old leaves of salt stressed-rice. Salt stress clearly up-regulated the expression of OsGDH2 and OsGDH3 in old leaves, while strongly down-regulated expression of OsGS2 and OsFd-GOGAT in old leaves., Conclusions: The down-regulation of OsGS2 and OsFd-GOGAT in old leaves might be a harmful response to excesses of Na+ and Cl-. Under salt stress, rice might accumulate Na+ and Cl- to toxic levels in old leaves. This might influence photorespiration process, reduce NH4+ production from photorespiration, and immediately down-regulate the expression of OsGS2 and OsFd-GOGAT in old leaves of salt stressed rice. Excesses of Na+ and Cl- also might change the pathway of NH4+ assimilation in old leaves of salt stressed rice plants, weaken GOGAT/GS pathway and elevate GDH pathway.

Background: Over application of phosphate fertilizers in modern agriculture contaminates waterways and disrupts natural ecosystems. Nevertheless, this is a common practice among farmers, especially in developing countries as abundant fertilizers are believed to boost crop yields. The study of plant phosphate metabolism and its underlying genetic pathways is key to discovering methods of efficient fertilizer usage. The work presented here describes a genome-wide resource on the molecular dynamics underpinning the response and recovery in roots and shoots of Arabidopsis thaliana to phosphate-starvation., Results: Genome-wide profiling by micro- and tiling-arrays (accessible from GEO: GSE34004) revealed minimal overlap between root and shoot transcriptomes suggesting two independent phosphate-starvation regulons. Novel gene expression patterns were detected for over 1000 candidates and were classified as either initial, persistent, or latent responders. Comparative analysis to AtGenExpress identified cohorts of genes co-regulated across multiple stimuli. The hormone ABA displayed a dominant role in regulating many phosphate-responsive candidates. Analysis of co-regulation enabled the determination of specific versus generic members of closely related gene families with respect to phosphate-starvation. Thus, among others, we showed that PHR1-regulated members of closely related phosphate-responsive families (PHT1;1, PHT1;7-9, SPX1-3, and PHO1;H1) display greater specificity to phosphate-starvation than their more generic counterparts., Conclusion: Our results uncover much larger, staged responses to phosphate-starvation than previously described. To our knowledge, this work describes the most complete genome-wide data on plant nutrient stress to-date.