The ERF11 Transcription Factor Promotes Internode Elongation by Activating Gibberellin Biosynthesis and Signaling.

The phytohormone gibberellin (GA) plays a key role in promoting stem elongation in plants. Previous studies show that GA activates its signaling pathway by inducing rapid degradation of DELLA proteins, GA signaling repressors. Using an activation-tagging screen in a reduced-GA mutant ga1-6 background, we identified AtERF11 to be a novel positive regulator of both GA biosynthesis and GA signaling for internode elongation. Overexpression of AtERF11 partially rescued the dwarf phenotype of ga1-6 AtERF11 is a member of the ERF (ETHYLENE RESPONSE FACTOR) subfamily VIII-B-1a of ERF/AP2 transcription factors in Arabidopsis (Arabidopsis thaliana). Overexpression of AtERF11 resulted in elevated bioactive GA levels by up-regulating expression of GA3ox1 and GA20ox genes. Hypocotyl elongation assays further showed that overexpression of AtERF11 conferred elevated GA response, whereas loss-of-function erf11 and erf11 erf4 mutants displayed reduced GA response. In addition, yeast two-hybrid, coimmunoprecipitation, and transient expression assays showed that AtERF11 enhances GA signaling by antagonizing the function of DELLA proteins via direct protein-protein interaction. Interestingly, AtERF11 overexpression also caused a reduction in the levels of another phytohormone ethylene in the growing stem, consistent with recent finding showing that AtERF11 represses transcription of ethylene biosynthesis ACS genes. The effect of AtERF11 on promoting GA biosynthesis gene expression is likely via its repressive function on ethylene biosynthesis. These results suggest that AtERF11 plays a dual role in promoting internode elongation by inhibiting ethylene biosynthesis and activating GA biosynthesis and signaling pathways.

PIL5, a phytochrome-interacting bHLH protein, regulates gibberellin responsiveness by binding directly to the GAI and RGA promoters in Arabidopsis seeds.

Previous work showed that PHYTOCHROME-INTERACTING FACTOR3-LIKE5 (PIL5), a light-labile basic helix-loop-helix protein, inhibits seed germination by repressing GIBBERELLIN 3beta-HYDROXYLASE1 (GA3ox1) and GA3ox2 and activating a gibberellic acid (GA) catabolic gene (GA2ox2). However, we show persistent light-dependent and PIL5-inhibited germination behavior in the absence of both de novo GA biosynthesis and deactivation by GA2ox2, suggesting that PIL5 regulates not only GA metabolism but also GA responsiveness. PIL5 increases the expression of two GA repressor (DELLA) genes, GA-INSENSITIVE (GAI) and REPRESSOR OF GA1-3 (RGA/RGA1), in darkness. The hypersensitivity of gai-t6 rga-28 to red light and the suppression of germination defects of a rga-28 PIL5 overexpression line show the significant role of this transcriptional regulation in seed germination. PIL5 also increases abscisic acid (ABA) levels by activating ABA biosynthetic genes and repressing an ABA catabolic gene. PIL5 binds directly to GAI and RGA promoters but not to GA and ABA metabolic gene promoters. Together, our results show that light signals perceived by phytochromes cause a reduction in the PIL5 protein level, which in turn regulates the transcription of two DELLA genes directly and that of GA and ABA metabolic genes indirectly.