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Huber, S.

Publications and source records attributed to Huber, S..

2 recordsLinked to original sources

Increased temperatures may safeguard the nutritional quality of crops under future elevated CO2 concentrations

Iron (Fe) and zinc (Zn) deficiencies are a global human health problem that may worsen by growth of crops at elevated atmospheric CO2 concentration (eCO2). However, climate change will also involve higher temperature, but it is unclear how the combined effect of eCO2 and higher temperature will affect the nutritional quality of food crops. To begin to address this question, we grew soybean (Glycine max) in a Temperature by Free-Air CO2 Enrichment (T-FACE) experiment in 2014 and 2015 under ambient (400 mol mol-1) and elevated (600 mol mol-1) CO2 concentration and under ambient and elevated temperatures (+2.7 {degrees}C day and +3.4 {degrees}C at night). In our study, eCO2 significantly decreased Fe concentration in soybean seeds in both seasons (-8.7% and -7.7%) and Zn concentration in one season (-8.9%) while higher temperature (at ambient CO2 concentration) had the opposite effect. The combination of eCO2 with elevated temperature generally restored seed Fe and Zn concentrations to levels obtained under ambient CO2 and temperature conditions, suggesting that the potential threat to human nutrition by increasing CO2 concentration may not be realized. In general, seed Fe concentration was negatively correlated with yield suggesting inherent limitations to increasing seed Fe. In addition, we confirm our previous report that the concentration of seed storage products and several minerals varies with node position at which the seeds developed. Overall, these results demonstrate the complexity of predicting climate change effects on food security when various environmental parameters change in an interactive manner.

plant biology

HtrA1 activation is driven by an allosteric mechanism of inter-monomer communication

The human protease family HtrA is responsible for preventing protein misfolding and mislocalization, and a key player in several cellular processes. Among these, HtrA1 is implicated in several cancers, cerebrovascular disease and age-related macular degeneration. HtrA1 activation, although very relevant for drug-targeting this protease, remains poorly characterized. Our work provides a mechanistic step-by-step description of HtrA1 activation and regulation. We report that the HtrA1 trimer is regulated by an allosteric mechanism by which monomers relay the activation signal to each other, in a PDZ-domain independent fashion. Notably, we show that inhibitor binding is precluded if HtrA1 monomers cannot communicate with each other. Our study establishes how HtrA1 oligomerization plays a fundamental role in proteolytic activity. Moreover, it offers a structural explanation for HtrA1-defective pathologies as well as mechanistic insights into the degradation of complex extracellular fibrils such as tubulin, amyloid beta and tau that belong to the repertoire of HtrA1.\n\nHighlightsO_LIMonomeric HtrA1 is activated by a gating mechanism.\nC_LIO_LITrimeric HtrA1 is regulated by PDZ-independent allosteric monomer cross-talk.\nC_LIO_LIHtrA1 oligomerization is key for proteolytic activity.\nC_LIO_LISubstrate-binding is precluded if monomers cannot communicate with each other.\nC_LI

biophysics