Leaf growth is a tightly regulated and complex process, which responds in a dynamic manner to changing environmental conditions, but the mechanisms that reduce growth under adverse conditions are rather poorly understood. We previously identified a growth inhibitory pathway regulating leaf growth upon exposure to a low concentration of mannitol and characterized the ETHYLENE RESPONSE FACTOR (ERF)/APETALA2 transcription factor ERF6 as a central activator of both leaf growth inhibition and induction of stress tolerance genes. Here, we describe the role of the transcriptional repressor ERF11 in relation to the ERF6-mediated stress response in Arabidopsis (Arabidopsis thaliana). Using inducible overexpression lines, we show that ERF6 induces the expression of ERF11. ERF11 in turn molecularly counteracts the action of ERF6 and represses at least some of the ERF6-induced genes by directly competing for the target gene promoters. As a phenotypical consequence of the ERF6-ERF11 antagonism, the extreme dwarfism caused by ERF6 overexpression is suppressed by overexpression of ERF11.Together, our data demonstrate that dynamic mechanisms exist to fine-tune the stress response and that ERF11 counteracts ERF6 to maintain a balance between plant growth and stress defense.Plants are constantly challenged to survive and maintain growth in changing environments. In natural environments, as well as in laboratories, growth conditions are rarely optimal, generating a weak but continuous stress. In such suboptimal conditions, the equilibrium between sustained plant growth and activation of stress defense mechanisms is defied and needs to be continuously rebalanced and fine-tuned (Claeys and Inzé, 2013).To unravel these growth-and defense-related mechanisms in Arabidopsis (Arabidopsis thaliana), researchers commonly use in vitro setups in which different growth inhibitory compounds are added to the growth medium (Verslues et al., 2006;Lawlor, 2013;Claeys et al., 2014). Mannitol, for example, is a frequently applied compound to induce mild stress because it results in both inhibition of leaf growth and activation of stress-responsive genes (Kreps et al., 2002;Skirycz et al., 2010Skirycz et al., , 2011Dubois et al., 2013;Claeys et al., 2014;Trontin et al., 2014). Two putative receptorlike kinases, ENHANCED GROWTH ON MANNITOL1 (EGM1) and EGM2, are presumably involved in the detection of mannitol and further downstream activation of the growth and tolerance responses (Trontin et al., 2014). Previously, we have shown that mannitolinduced responses are specific to the different stages of Arabidopsis leaf development (Skirycz et al., 2010). In very young Arabidopsis leaves, in which cells are not yet expanding but still actively dividing, exposure to mannitol triggers the accumulation of the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) and the transcriptional induction of ethylene-related genes. Interestingly, these responses are extremely fast, with several ETHYLENE RESPONSE FACTORs (ERFs; ERF1, ERF2, ERF5, ERF6, and ERF11...
