The length of the Arabidopsis thaliana life cycle depends on the timing of the floral transition. Here, we define the relationship between the plant stress hormone ethylene and the timing of floral initiation. Ethylene signaling is activated by diverse environmental stresses, but it was not previously clear how ethylene regulates flowering. First, we show that ethylene delays flowering in Arabidopsis, and that this delay is partly rescued by loss-of-function mutations in genes encoding the DELLAs, a family of nuclear gibberellin (GA)-regulated growth-repressing proteins. This finding suggests that ethylene may act in part by modulating DELLA activity. We also show that activated ethylene signaling reduces bioactive GA levels, thus enhancing the accumulation of DELLAs. Next, we show that ethylene acts on DELLAs via the CTR1-dependent ethylene response pathway, most likely downstream of the transcriptional regulator EIN3. Ethylene-enhanced DELLA accumulation in turn delays flowering via repression of the floral meristem-identity genes LEAFY (LFY) and SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1). Our findings establish a link between the CTR1/EIN3-dependent ethylene and GA-DELLA signaling pathways that enables adaptively significant regulation of plant life cycle progression in response to environmental adversity.floral transition ͉ Arabidopsis thaliana ͉ LFY ͉ gibberellin F loral initiation is a major step in the plant life cycle (1). Accordingly, plants have evolved mechanisms for regulating the timing of floral initiation. These mechanisms permit an adaptively significant integrated response to multiple interacting factors (both internal and external to the plant). In essence, the endogenous developmental competence of plants to flower is integrated with environmental cues that signal the onset of conditions favorable for reproductive success (2).In this article, we describe the role of the gaseous phytohormone ethylene in the regulation of floral initiation. Ethylene is already known to modulate Arabidopsis vegetative environmental growth responses (3-5). For example, adverse environmental conditions enhance ethylene production, and thereby restrain growth (3, 4). Ethylene is perceived by the ETR1 family of ethylene receptors (6-10). In the absence of ethylene, ETR1 activates CTR1, a Ser/Thr kinase (closely related to the RAF kinases) that is a negative regulator of ethylene signaling (11,12). Downstream of CTR1 are several positive regulators of ethylene response: EIN2 (a membrane-associated protein whose function is not clear; ref. 13) and the EIN3 and EIN3-like (EIL) transcription factors (14, 15). EIN3 regulates ethylene-responsive genes (6, 15), whereas overexpression of EIN3 results in the constitutive activation of ethylene responses (14). Furthermore, ethylene response depends on EIN3 stability. In the absence of ethylene, EIN3 degradation is promoted by a specific Skp1-cullin-F box protein (SCF) E3 ubiquitin ligase (SCF EBF1/EBF2 ) that targets EIN3 for destruction by the proteasome (16-18). Howev...