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Mitigation potential of urban greening during heatwaves and stormwater events: a modeling study for Karlsruhe, Germany
Abstract Climate change is increasing the frequency and intensity of urban heat islands and stormwater flooding. In order to mitigate these threats cities are turning toward green infrastructure to restore the hydrologic cycle in a way that increases the ecosystem services provided by trees. Strategically designed green infrastructure can mitigate runoff volume by rainfall interception through tree canopies and redirect impervious runoff into bioswales that promote infiltration. In addition, urban greens mitigate extreme heat via evapotranspiration and shading. Here we applied the i-Tree HydroPlus model to the German city of Karlsruhe and its twenty-seven districts with varying initial conditions of tree cover to analyze the potential for both runoff and heat mitigation during dry and wet periods throughout a 5-year period. After analyzing initial tree cover and drainage conditions, we used the model to simulate a green infrastructure scenario for each district with restored hydrology and tree cover at 30%. Regarding trade-offs between runoff and heat mitigation, the results confirm that dry soils before storm events lead to greater runoff reduction by 10%, and wet soils prior to heatwaves resulted in a greater evaporative cooling. Compared to current conditions, the green infrastructure scenarios resulted in decreasing the number of extreme heat hours (Heat Index > 31 °C) per year on average by 64.5%, and to reduce runoff in average by 58% across all city districts. Thus, our simulation results show that investing into a greener infrastructure, has positive impacts on microclimate and hydrology. Finally, we discuss synergies and trade-offs of the investigated management options as well as the transferability of results to other cities.
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C-terminal amides mark proteins for degradation via SCF–FBXO31
Abstract During normal cellular homeostasis, unfolded and mislocalized proteins are recognized and removed, preventing the build-up of toxic byproducts 1 . When protein homeostasis is perturbed during ageing, neurodegeneration or cellular stress, proteins can accumulate several forms of chemical damage through reactive metabolites 2,3 . Such modifications have been proposed to trigger the selective removal of chemically marked proteins 3–6 ; however, identifying modifications that are sufficient to induce protein degradation has remained challenging. Here, using a semi-synthetic chemical biology approach coupled to cellular assays, we found that C-terminal amide-bearing proteins (CTAPs) are rapidly cleared from human cells. A CRISPR screen identified FBXO31 as a reader of C-terminal amides. FBXO31 is a substrate receptor for the SKP1–CUL1–F-box protein (SCF) ubiquitin ligase SCF–FBXO31, which ubiquitylates CTAPs for subsequent proteasomal degradation. A conserved binding pocket enables FBXO31 to bind to almost any C-terminal peptide bearing an amide while retaining exquisite selectivity over non-modified clients. This mechanism facilitates binding and turnover of endogenous CTAPs that are formed after oxidative stress. A dominant human mutation found in neurodevelopmental disorders reverses CTAP recognition, such that non-amidated neosubstrates are now degraded and FBXO31 becomes markedly toxic. We propose that CTAPs may represent the vanguard of a largely unexplored class of modified amino acid degrons that could provide a general strategy for selective yet broad surveillance of chemically damaged proteins.