Involvement of COP1 in ethylene- and light-regulated hypocotyl elongation

Abstract

Ethylene and light act through specific signal transduction mechanisms to coordinate the development of higher plants. Application of 1-aminocyclopropane-1-carboxylic acid (ACC, an ethylene precursor) suppresses the hypocotyl elongation of Arabidopsis seedlings in dark, but stimulates it in light. However, the mechanisms of opposite effects of ethylene on hypocotyl elongation in light and dark remain unclear. In the present study, we investigated the key factors involved in the opposite effects of ethylene on hypocotyl elongation in Arabidopsis seedlings. The effects of ACC on hypocotyl elongation of IAA-insensitive mutants including tir1-1, axr1-3, and axr1-12 seedlings were reduced in light but not in dark. The DR5 promoter, a synthetic auxin-response promoter, was used to quantify the level of IAA responses. There was a marked increase in DR5-GFP signals in response to ACC treatment in hypocotyls of DR5-GFP seedlings in light, but not in dark. CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) is an important downstream component of light signaling. ETHYLENE-INSENSITIVE3 (EIN3, an ethylene-stabilized transcription factor) directly regulates ETHYLENE-RESPONSE-FACTOR1 (ERF1). The cop1-4 mutant treated with ACC and cop1-4/EIN3ox plants developed long hypocotyls in darkness. Expression of ERF1 in the cop1-4 mutant was induced by ACC treatment in dark, but the expression of ERF1 in the wild type was not affected. Taken together, ethylene-promoting hypocotyl via IAA is mediated by light, and COP1 has a significant impact on the transcription of some genes downstream of EIN3. Thus, COP1 plays a crucial role in the opposite effects of ethylene on hypocotyl elongation.