Genetic and epigenetic basis of phytohormonal control of floral transition in plants.

The timing of the developmental transition from the vegetative to the reproductive stage is critical for angiosperms, and is fine-tuned by the integration of endogenous factors and external environmental cues to ensure successful reproduction. Plants have evolved sophisticated mechanisms to response to diverse environmental or stress signals, and these can be mediated by hormones to coordinate flowering time. Phytohormones such as gibberellin, auxin, cytokinin, jasmonate, abscisic acid, ethylene, and brassinosteroids and the cross-talk among them are critical for the precise regulation of flowering time. Recent studies of the model flowering plant Arabidopsis have revealed that diverse transcription factors and epigenetic regulators play key roles in relation to the phytohormones that regulate floral transition. This review aims to summarize our current knowledge of the genetic and epigenetic mechanisms that underlie the phytohormonal control of floral transition in Arabidopsis, offering insights into how these processes are regulated and their implications for plant biology.

A pair of nuclear factor Y transcription factors act as positive regulators in jasmonate signaling and disease resistance in Arabidopsis.

The plant hormone jasmonate (JA) regulates plant growth and immunity by orchestrating a genome-wide transcriptional reprogramming. In the resting stage, JASMONATE-ZIM DOMAIN (JAZ) proteins act as main repressors to regulate the expression of JA-responsive genes in the JA signaling pathway. However, the mechanisms underlying de-repression of JA-responsive genes in response to JA treatment remain elusive. Here, we report two nuclear factor Y transcription factors NF-YB2 and NF-YB3 (thereafter YB2 and YB3) play key roles in such de-repression in Arabidopsis. YB2 and YB3 function redundantly and positively regulate plant resistance against the necrotrophic pathogen Botrytis cinerea, which are specially required for transcriptional activation of a set of JA-responsive genes following inoculation. Furthermore, YB2 and YB3 modulated their expression through direct occupancy and interaction with histone demethylase Ref6 to remove repressive histone modifications. Moreover, YB2 and YB3 physically interacted with JAZ repressors and negatively modulated their abundance, which in turn attenuated the inhibition of JAZ proteins on the transcription of JA-responsive genes, thereby activating JA response and promoting disease resistance. Overall, our study reveals the positive regulators of YB2 and YB3 in JA signaling by positively regulating transcription of JA-responsive genes and negatively modulating the abundance of JAZ proteins.