MiR160 and its target genes ARF10, ARF16 and ARF17 modulate hypocotyl elongation in a light, BRZ, or PAC-dependent manner in Arabidopsis: miR160 promotes hypocotyl elongation.

Multiple hormonal and environmental signals participate in the regulation of plant hypocotyl elongation, which allow the plants to optimize their survival strategy from seed germination to seedling establishment. Auxin plays key roles in cell elongation via auxin signaling transduction and its interactions with other hormonal and environmental signals. However, the roles of auxin response factor (ARF) family in cross-talk between auxin and other hormonal or environmental signals during hypocotyl elongation are not fully understood. Here we show that miR160 and its target genes ARF10, ARF16 and ARF17 modulate hypocotyl elongation in a light, brassinazole (BRZ, a BR biosynthesis inhibitor), or paclobutrazol (PAC, a GA biosynthesis inhibitor)-dependent manner in Arabidopsis. miR160, ARF10, ARF16 and ARF17 have no effects on hypocotyl elongation in the dark. However, in the presence of either light, BRZ, or PAC, ARF10, ARF16 and ARF17 inhibit hypocotyl elongation, and miR160 promotes hypocotyl elongation via cleavage of their mRNA. miR160 and ARF10 are both expressed in the hypocotyl. ARF10 represses the expression of PACLOBUTRAZOL RESISTANCE1 (PRE1) and 35S::PRE1 could partly rescue the phenotype of mARF10 (a miR160-resistant form of ARF10), suggesting that PRE1 acts downstream of ARF10 in regulating hypocotyl elongation. In conclusion, our results indicate that miR160-ARF10/16/17 might serve as a molecular link in cross-talk of auxin, light, BR, and GA in hypocotyl elongation.