HY5 regulates light-responsive transcription of microRNA163 to promote primary root elongation in Arabidopsis seedlings

MicroRNAs(miRNAs)play key roles in the post-transcriptional regulation of gene expression in plants.Many miRNAs are responsive to environmental signals.Light is the first environmental signal perceived by plants after emergence from the soil.However,less is known about the roles and regulatory mechanism of miRNAs in response to light signal.Here,using small RNA sequencing,we determined that miR163 is significantly rapidly induced by light signaling in Arabidopsis thaliana seedlings.The light-inducible response of miR163 functions genetically downstream of LONG HYPOCOTYL 5(HY5),a central positive regulator of photomorphogenesis.HY5 directly binds to the two G/C-hybrid elements in the miR163 promoter with unequal affinity;one of these elements,which is located next to the transcription start site,plays a major role in light-induced expression of miR163.Overexpression of miR163 rescued the defective primary root elongation of hy5 seedlings without affecting lateral root growth,whereas overexpressing of miR163 target PXMT1 inhibited primary root elongation.These findings provide insight into understanding the post-transcriptional regulation of root photomorphogenesis mediated by the HY5-miR163-PXMT1 network.

SICKLE represses photomorphogenic development of Arabidopsis seedlings via HY5-and PIF4-mediated signaling

Arabidopsis CONSTITUTIVELY PHOTOMORPHO GENIC1(COP1)and PHYTOCHROME INTERACTING FACTORs(PIFs)are negative regulators,and ELONGATED HYPOCOTYL5(HY5)is a positive regulator of seedling photomorphogenic development.Here,we report that SICKLE(SIC),a proline rich protein,acts as a novel negative regulator of photomorphogenesis.HY5 directly binds the SIC promoter and activates SIC expression in response to light.In turn,SIC physically interacts with HY5 and interferes with its transcriptional regulation of downstream target genes.Moreover,SIC interacts with PIF4 and promotes PIF4-activated transcription of itself.Interestingly,SIC is targeted by COP1 for 26S proteasomemediated degradation in the dark.Collectively,our data demonstrate that light-induced SIC functions as a brake to prevent exaggerated light response via mediating HY5 and PIF4 signaling,and its degradation by COP1 in the dark avoid too strong inhibition on photomorphogenesis at the beginning of light exposure.