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Evers, J.

Publications and source records attributed to Evers, J..

2 recordsLinked to original sources

Identifying and quantifying the contribution of maize plant traits to nitrogen uptake and use through plant modelling

Breeding for high nitrogen use efficient crops can contribute to maintaining or even increasing yield with less nitrogen. Nitrogen use is co-determined by N uptake and physiological use efficiency (PE, biomass per unit of N taken up), to which soil processes as well as plant architectural, physiological and developmental traits contribute. The relative contribution of these crop traits to N use is not well known but relevant to identify breeding targets in important crop species like maize. To quantify the contribution of component plant traits to maize N uptake and use, we used a functional-structural plant model. We evaluated the effect of varying both shoot and root traits on crop N uptake across a range of nitrogen levels. Root architectural traits were found to play a more important role in root N uptake than physiological traits. Phyllochron determined the structure of the shoot through changes in source: sink ratio over time which, in interaction with light and temperature, resulted in a significant effect on PE and N uptake. Photosynthesis traits were more relevant to biomass accumulation rather than yield, especially under high nitrogen conditions. The traits identified in this study are potential targets in maize breeding for improved crop N uptake and use. HighlightOur research provides insight into the relevance of a range of traits for maize N uptake and N use, and identifies several potential target traits based on underlying mechanisms to assist maize breeding.

plant biology↗

Micromotion derived fluid shear stress mediates peri-electrode gliosis through mechanosensitive ion channels

Clinical applications for neural implant technologies are steadily advancing. Yet, despite clinical successes, neuroelectrode-based therapies require invasive neurosurgery and can subject local soft-tissues to micro-motion induced mechanical shear, leading to the development of peri-implant scaring. This reactive glial tissue creates a physical barrier to electrical signal propagation, leading to loss of device function. Although peri-electrode gliosis is a well described contributor to neuroelectrode failure, the mechanistic basis behind the initiation and progression of glial scarring remains poorly understood. Here, we develop an in silico model of electrode-induced shear stress to evaluate the evolution of the peri-electrode fluid-filled void, encompassing a solid and viscoelastic liquid/solid interface. This model was subsequently used to inform an in vitro parallel-plate flow model of micromotion mediated peri-electrode fluid shear stress. Ventral mesencephalic E14 rat embryonic in vitro cultures exposed to physiologically relevant fluid shear exhibited upregulation of gliosis-associated proteins and the overexpression of two mechanosensitive ion channel receptors, PIEZO1 and TRPA1, confirmed in vivo in a neural probe induced rat glial scar model. Finally, it was shown in vitro that chemical inhibition/activation of PIEZO1 could exacerbate or attenuate astrocyte reactivity as induced by fluid shear stress and that this was mitochondrial dependant. Together, our results suggests that mechanosensitive ion channels play a major role in the development of the neuroelectrode micromotion induced glial scar and that the modulation of PIEZO1 and TRPA1 through chemical agonist/antagonist may promote chronic electrode stability in vivo. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=144 SRC="FIGDIR/small/523766v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@962f03org.highwire.dtl.DTLVardef@1e8a6adorg.highwire.dtl.DTLVardef@116cbb6org.highwire.dtl.DTLVardef@19830da_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIPeri-electrode void progression is mediated by fluid flow shear stress C_LIO_LIOscillatory fluid flow shear stress replicates neuroelectrode glial scarring in vitro C_LIO_LIAstrocyte PIEZO1 and TRPA1 are upregulated at the peri-electrode region in response to electrode micromotion C_LIO_LIPIEZO1 pharmaceutical activation diminishes shear stress-induced gliosis C_LIO_LIPIEZO1 chemical inhibition exacerbates gliosis and reduces mitochondrial functions C_LI

neuroscience↗