Models of vegetation function are widely used to predict the effects of climate change on carbon, water and nutrient cycles of terrestrial ecosystems, and their feedbacks to climate. Stomatal conductance, the process that governs plant water use and carbon uptake, is fundamental to such models. In this paper, we reconcile two long-standing theories of stomatal conductance. The empirical approach, which is most commonly used in vegetation models, is phenomenological, based on experimental observations of stomatal behaviour in response to environmental conditions. The optimal approach is based on the theoretical argument that stomata should act to minimize the amount of water used per unit carbon gained. We reconcile these two approaches by showing that the theory of optimal stomatal conductance can be used to derive a model of stomatal conductance that is closely analogous to the empirical models. Consequently, we obtain a unified stomatal model which has a similar form to existing empirical models, but which now provides a theoretical interpretation for model parameter values. The key model parameter, g 1 , is predicted to increase with growth temperature and with the marginal water cost of carbon gain. The new model is fitted to a range of datasets ranging from tropical to boreal trees. The parameter g 1 is shown to vary with growth temperature, as predicted, and also with plant functional type. The model is shown to correctly capture responses of stomatal conductance to changing atmospheric CO 2 , and thus can be used to test for stomatal acclimation to elevated CO 2 . The reconciliation of the optimal and empirical approaches to modelling stomatal conductance is important for global change biology because it provides a simple theoretical framework for analyzing, and simulating, the coupling between carbon and water cycles under environmental change.

Summary• Data from 13 long-term (> 1 yr), field-based studies of the effects of elevated CO 2 concentration ([CO 2 ]) on European forest tree species were analysed using meta-analysis and modelling. Meta-analysis was used to determine mean responses across the data sets, and data were fitted to two commonly used models of stomatal conductance in order to explore response to environmental conditions and the relationship with assimilation.• Meta-analysis indicated a significant decrease (21%) in stomatal conductance in response to growth in elevated [CO 2 ] across all studies. The response to [CO 2 ] was significantly stronger in young trees than old trees, in deciduous compared to coniferous trees, and in water stressed compared to nutrient stressed trees. No evidence of acclimation of stomatal conductance to elevated [CO 2 ] was found.• Fits of data to the first model showed that growth in elevated [CO 2 ] did not alter the response of stomatal conductance to vapour pressure deficit, soil water content or atmospheric [CO 2 ]. Fits of data to the second model indicated that conductance and assimilation responded in parallel to elevated [CO 2 ] except when water was limiting.• Data were compared to a previous meta-analysis and it was found that the response of g s to elevated [CO 2 ] was much more consistent in long-term (> 1 yr) studies, emphasising the need for long-term elevated [CO 2 ] studies. By interpreting data in terms of models, the synthesis will aid future modelling studies of responses of forest trees to elevated [CO 2 ].

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The chemopreventive agent sulforaphane is an isothiocyanate derived from cruciferous vegetables. Sulforaphane exerts cancer chemopreventive effects by inducing antioxidant/electrophile response element (ARE)-regulated phase 2 enzyme and antioxidant genes through activation of the transcription factor nuclear factor-E2-related factor 2 (Nrf2), which is regulated by the thiol-rich sensor protein Kelch-like ECH-associated protein 1 (Keap1). Sulforaphane is an electrophile that can react with protein thiols to form thionoacyl adducts. We hypothesized that, like other electrophilic Nrf2 activators, sulforaphane activates this system through specific modifications of the Keap1 protein. However, thionoacyl adducts are labile to hydrolysis and transacylation reactions, which complicate the identification of the sulforaphane adduct sites on Keap1. In this study, we characterized the stability of sulforaphane thionoacyl adducts and developed a liquid chromatography-tandem mass spectrometry method to map labile sulforaphane adduct sites formed on Keap1 in vitro. Sulforaphane displays a distinctly different pattern of Keap1 modification than previously studied ARE inducers that modify Keap1 by alkylation. Sulforaphane modified Keap1 most readily in the Kelch domain, rather than in the central linker domain, which is targeted by previously characterized ARE inducers. Also, in contrast to previously studied ARE inducers and as reported recently [Zhang, et al. (2005) J. Biol. Chem. 280, 30091-30099], sulforaphane treatment in vivo does not lead to the accumulation of ubiquitinated Keap1. Our observations suggest a novel mechanism for Nrf2 stabilization by sulforaphane-Keap1 thionoacyl adduct formation.

Activation of the transcription factor Nrf2 regulates expression of phase II enzymes and other adaptive responses to electrophile and oxidant stress. Nrf2 concentrations are regulated by the thiol-rich sensor protein Keap1, which is an adaptor protein for Cul3-dependent ubiquitination and degradation of Nrf2. However, the links between site specificity of Keap1 modification by electrophiles and mechanisms of Nrf2 activation are poorly understood. We studied the actions of the prototypical Nrf2 inducer tert-butylhydroquinone (

BackgroundCumulative oxidative damage is implicated in the pathogenesis of age-related macular degeneration (AMD). Nuclear factor erythroid 2-related factor 2 (NRF2) is a transcription factor that plays key roles in retinal antioxidant and detoxification responses. The purposes of this study were to determine whether NRF2-deficient mice would develop AMD-like retinal pathology with aging and to explore the underlying mechanisms.Methods and FindingsEyes of both wild type and Nrf2−/− mice were examined in vivo by fundus photography and electroretinography (ERG). Structural changes of the outer retina in aged animals were examined by light and electron microscopy, and immunofluorescence labeling. Our results showed that Nrf2−/− mice developed age-dependent degenerative pathology in the retinal pigment epithelium (RPE). Drusen-like deposits, accumulation of lipofuscin, spontaneous choroidal neovascularization (CNV) and sub-RPE deposition of inflammatory proteins were present in Nrf2−/− mice after 12 months. Accumulation of autophagy-related vacuoles and multivesicular bodies was identified by electron microcopy both within the RPE and in Bruch's membrane of aged Nrf2−/− mice.ConclusionsOur data suggest that disruption of Nfe2l2 gene increased the vulnerability of outer retina to age-related degeneration. NRF2-deficient mice developed ocular pathology similar to cardinal features of human AMD and deregulated autophagy is likely a mechanistic link between oxidative injury and inflammation. The Nrf2−/− mice can provide a novel model for mechanistic and translational research on AMD.