Expression of turtle riboflavin-binding protein represses mitochondrial electron transport gene expression and promotes flowering in Arabidopsis

BACKGROUND: Recently we showed that de novo expression of a turtle riboflavin-binding protein (RfBP) in transgenic Arabidopsis increased H(2)O(2) concentrations inside leaf cells, enhanced the expression of floral regulatory gene FD and floral meristem identity gene AP1 at the shoot apex, and induced early flowering. Here we report that RfBP-induced H(2)O(2) presumably results from electron leakage at the mitochondrial electron transport chain (METC) and this source of H(2)O(2) contributes to the early flowering phenotype. RESULTS: While enhanced expression of FD and AP1 at the shoot apex was correlated with early flowering, the foliar expression of 13 of 19 METC genes was repressed in RfBP-expressing (RfBP(+)) plants. Inside RfBP(+) leaf cells, cytosolic H(2)O(2) concentrations were increased possibly through electron leakage because similar responses were also induced by a known inducer of electron leakage from METC. Early flowering no longer occurred when the repression on METC genes was eliminated by RfBP gene silencing, which restored RfBP(+) to wild type in levels of FD and AP1 expression, H(2)O(2), and flavins. Flowering was delayed by the external riboflavin application, which brought gene expression and flavins back to the steady-state levels but only caused 55% reduction of H(2)O(2) concentrations in RfBP(+) plants. RfBP-repressed METC gene expression remedied the cytosolic H(2)O(2) diminution by genetic disruption of transcription factor NFXLl and compensated for compromises in FD and AP1 expression and flowering time. By contrast, RfBP resembled a peroxisomal catalase mutation, which augments the cytosolic H(2)O(2), to enhance FD and AP1 expression and induce early flowering. CONCLUSIONS: RfBP-repressed METC gene expression potentially causes electron leakage as one of cellular sources for the generation of H(2)O(2) with the promoting effect on flowering. The repressive effect on METC gene expression is not the only way by which RfBP induces H(2)O(2) and currently unappreciated factors may also function under RfBP(+) background. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12870-014-0381-5) contains supplementary material, which is available to authorized users.